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    APIGENIN 200:1

    Rated 5.00 out of 5 based on 7 customer ratings
    (7 customer reviews)

    $250.00

    Categories: Exclusive Products, Featured Tags: Adult Neurogenesis, Anti Alzheimer’s, Anti Cancer, Anti Diabetic Effects, Anti Obesity Effects, Appetite Suppressant, Boost nad+ by blocking key enzyme CD38, Enhances Memory, NMDA Antagonist, Powerful Anti Anxiety Effects, Powerful Anti Depressant Effects, Prevent Age Related Testosterone Decline, Protect Liver from Alcohol, Restore Youthful Skin, The Strongest Apigenin on the Planet
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    Apigenin 200:1

    100g $250 300 1/8 tsp servings

    Dosage: Start 1 tsp a day first 2 weeks then you can move down to 1/2 tsp a day for 2 weeks then 1/4 tsp a day for 2 weeks then 1/8 tsp as needed.

     

    the strongest Apigenin on the planet 

    Want to grow some new brain cells?
    It’s called adult neurogenesis; keep reading.

     

    Apigenin and related compounds stimulate adult neurogenesis

    “Apigenin and related compounds stimulate adult neurogenesis in vivo and in vitro, by promoting neuronal differentiation. Apigenin promotes learning and memory performance in the Morris water task. The application claims the use of apigenin and related compounds for stimulating adult neurogenesis and for the treatment of neurological diseases, disorders and injuries, by stimulating the generation of neuronal cells in the adult brain.”

    “For most of the twentieth century, there was a general consensus that brain cells could not renew themselves once the developmental period was over. Then, especially over the last two decades, overwhelming evidence gradually accumulated for the capacity of new neurons to be born in the adult brain in two clearly defined locations: the subventricular zone and the dentate gyrus (DG) of the hippocampus. The hippocampus is well known to play important roles in learning and memory, and this adult DG neurogenesis has not only been implicated in memory but has led to ideas that it could be harnessed to treat neurodegenerative and neuropsychiatric disorders.”

    https://www.tandfonline.com/doi/full/10.1517/13543770902721279?scroll=top&needAccess=true

    Plant compound found in spices, herbs increases brain connections

    Flavonoid apigenin has potential to treat diseases like schizophrenia, depression, Alzheimer’s and Parkinson’s

    “Apigenin, a substance found in parsley, thyme, chamomile and red pepper, improves neuron formation and strengthens the connections between brain cells, new lab research demonstrates.”

    New approach in treatment of brain injury: Neurotrophic effects of Apigenin

    “Brain injury initiates a neuroinflammatory cascade that contributes to substantial neuronal damage. Administration of lipopolysaccharide (LPS) impaired antioxidant mechanisms, increased peroxidation and impaired mitochondrial redox activity causing brain inflammation as well as neuronal damage and impairment of brain monoamines. Apigenin gathered extensive attention in recent years because of its chemopreventive, antioxidant and antiinflammatory effects. This study aimed to evaluate the impact of apigenin in LPS induced brain injury in experimental rats and to evaluate its role in monoamines regulation as well as DNA damage reduction. Forty male albino rats were used in this study, divided into four groups (control, apigenin, LPS and treated groups). Brain malondialdehyde (MDA), brain nitric oxide (NO) and serum paraoxnase activity (PON-1) were estimated colorimeterically. DNA damage was evaluated by comet assay method, in addition to brain monoamines assessment by HPLC. Histopathological and Immunohistochemistry of cyclooxygenases (COX-1, COX-2) were also performed. The data showed that lipopolysaccharide significantly increased brain MDA, NO and monoamines concomitant with a reduction in PON-1. Contrarily, apigenin supplementation improved these values in treated group. The present study provides insights into the design of flavonoid with optimal neuroprotective activities.”

    POTENT SASP INHIBITOR


    During senescence, cells express molecules called senescence-associated secretory phenotype (SASP), including growth factors, proinflammatory cytokines, chemokines, and proteases. The SASP induces a chronic low-grade inflammation adjacent to cells and tissues, leading to degenerative diseases. The anti- inflammatory activity of flavonoids was investigated on SASP expression in senescent fibroblasts. Effects of flavonoids on SASP expression such as IL-1a, IL-1b, IL-6, IL-8, GM-CSF, CXCL1, MCP-2 and MMP-3 and signaling molecules were examined in bleomycin-induced senescent BJ cells. In vivo activity of apigenin on SASP suppression was identified in the kidney of aged rats. Among the five naturally-occurring flavonoids initially tested, apigenin and kaempferol strongly inhibited the expression of SASP. These flavonoids inhibited NF-kB p65 activity via the IRAK1/IkBa signaling pathway and expression of IkBz. Blocking IkBz expression especially reduced the expression of SASP. A structure-activity relationship study using some synthetic flavones demonstrated that hydroxyl substitutions at C-20,30,40,5 and 7 were important in inhibiting SASP production. Finally, these results were verified by results showing that the oral administration of apigenin significantly reduced elevated levels of SASP and IkBz mRNA in the kidneys of aged rats. This study is the first to show that certain flavonoids are inhibitors of SASP production, partially related to NF-kB p65 and IkBz signaling pathway, and may effectively protect or alleviate chronic low-grade inflammation in degenerative diseases such as cardiovascular diseases and late-stage cancer. Inhibitory activity of apigenin on IL-6, IL-8, and IL-1b was the most potent among the five flavonoids that were tested (86.5%, 60.9%, and 94.9% at 10 mM, respectively).

    Apigenin and preventing/reversing alcohol liver injury.

    “In conclusion, our present results demonstrate that apigenin can exert an inhibitory effect on ethanol-induced oxidative stress and LPS-induced inflammatory response in the cultured BRL cells, and its mechanisms may be related to the reduction of CYP2E1 expression, increment of antioxidant ability, and regulation of inflammatory gene expression. These effects of apigenin may be good for the prevention and treatment of alcoholic liver injury.”

    https://www.sciencedirect.com/science/article/pii/S1214021X1730162X

     

    You want high NAD+ levels. ( CD38 is a key enzyme involved in the degradation of NAD+) Apigenin blocks CD38.

    Flavonoid apigenin is an inhibitor of the NAD+ ase CD38: implications for cellular NAD+ metabolism, protein acetylation, and treatment of metabolic syndrome

    “Metabolic syndrome is a growing health problem worldwide. It is therefore imperative to develop new strategies to treat this pathology. In the past years, the manipulation of NAD+ metabolism has emerged as a plausible strategy to ameliorate metabolic syndrome. In particular, an increase in cellular NAD+ levels has beneficial effects, likely because of the activation of sirtuins. Previously, we reported that CD38 is the primary NAD+ase in mammals. Moreover, CD38 knockout mice have higher NAD+ levels and are protected against obesity and metabolic syndrome. Here, we show that CD38 regulates global protein acetylation through changes in NAD+ levels and sirtuin activity. In addition, we characterize two CD38 inhibitors: quercetin and apigenin. We show that pharmacological inhibition of CD38 results in higher intracellular NAD+ levels and that treatment of cell cultures with apigenin decreases global acetylation as well as the acetylation of p53 and RelA-p65. Finally, apigenin administration to obese mice increases NAD+ levels, decreases global protein acetylation, and improves several aspects of glucose and lipid homeostasis.”

    http://diabetes.diabetesjournals.org/content/early/2012/11/18/db12-1139.short

    “Scientists are discovering new ways that NAD+ facilitates healthy longevity.

    NAD+ levels markedly decline with age, creating an energy deficit that decreases the body’s ability to retain youthful function.

    To give you an idea how impactful NAD+ can be, by age 50 a typical person may have only half the NAD+ they did in youth. By age 80, NAD+ levels drop to only 1% to 10% expressed in youth.

    Deficiency of NAD+ predisposes us to accelerated aging and impedes our ability to fully benefit from resveratrol.

    http://www.lifeextension.com/Magazine/2018/2/Anti-Aging-Effects-Of-NAD/Page-01

     

    Apigenin prevents age related testosterone decline.

    (APIGENIN) : Decreases COX2 while increasing StAR thus suppressing age related testosterone decline.
    “During the course of male aging, circulating levels of testosterone decline [1, 2], resulting in decreases in muscle function, bone density, sex function and other physiological functions [3-5]. It was also observed that serum testosterone concentrations were significantly lower in men with Alzheimer’s disease in comparison to non-demented and age-matched men [6, 7]. Supplementation with testosterone reduced β-amyloid peptide and hyperphosphorylation of τ protein, two bio-markers of the disease [8-10]. The studies suggested that low blood testosterone is a possible risk factor for development of Alzheimer’s disease [11]. To improve the health of aging males, especially those suffering from age-associated hypogonadism, we have been attempting to determine if it is possible to delay the age-related decline in blood testosterone concentration.

    Testosterone is mainly synthesized in testicular Leydig cells from substrate cholesterol and then released into the circulation [12]. It is known that the levels of blood testosterone are affected by multiple physiological and biochemical factors associated with aging [13]. It has also been shown that the primary site for the decline in blood testosterone appears to be at the level of testosterone biosynthesis in aging Leydig cells [14]. The rate-limiting step in testosterone biosynthesis is the transfer of the substrate cholesterol from the outer to the inner mitochondrial membrane to initiate the steroidogenic process [15]. Previous studies reported that a newly synthesized protein induced by trophic hormone, namely the steroidogenic acute regulatory (StAR) protein, plays a critical function at this step by facilitating the mitochondrial cholesterol transfer [16-18]. A large body of evidence demonstrated that the levels of StAR protein expression strongly affect testosterone production in Leydig cells [19]. However, StAR protein expression also decreases during the course of Leydig cell aging, and the cholesterol supply to the mitochondrial inner membrane is reduced in aged Leydig cells [20-22]. These studies implicated the involvement of an age-related decline in StAR gene expression in the decrease in testosterone production.

    In addition, our studies have demonstrated that expression of cyclooxygenase-2 (COX2, an isoform of cyclooxygenase) increases during Leydig cell aging, a process that enhances the COX2-dependent inhibition of StAR gene expression. Consequently, the age-related increase in COX2 results in decreases in StAR gene expression and testosterone biosynthesis. When COX2 activity was inhibited, StAR protein expression and testosterone production were increased. Moreover, feeding aged rats with a selective COX2 inhibitor reversed the decreased StAR protein and blood testosterone concentration [23, 24].

    Further studies showed that the observed COX2-dependent inhibition of StAR gene expression involves the negative signaling through an autocrine loop consisting of COX2-thromboxane A synthase (TBXAS)-thromboxane A2 (TBX A2)-receptor, in which TBX A2 generated by the co-action of COX2 and TBXAS is released from Leydig cells, and then binds to its receptors [25, 26]. These studies further indicated that the TBX A2-receptor complex regulate the expression or stability of DAX-1 (dosage sensitive sex reversal-adrenal hypoplasia congenita critical region on the X chromosome, gene-1) protein, a transcriptional repressor of StAR gene expression. Blocking the COX2-dependent signaling through this loop reduced DAX-1 protein and increased the sensitivity of Leydig cells to trophic hormone stimulation, resulting in dramatic increases in StAR gene expression and testosterone production in aged Leydig cells. These studies suggested that it is possible to delay the age-related decline in testosterone production by interrupting the signaling through this loop at any step, by either inhibiting the activity of COX2 or TBXAS, or by blocking the TBX A2 receptor.

    We have continued the studies in an attempt to identify natural compounds in food or food supplements that could enhance StAR gene expression in Leydig cells by intervention in the mechanism.
    After screening a group of compounds, the present study identified a natural flavonoid, apigenin that interrupted the COX2-dependent signaling by blocking the TBX A2 receptor and increased StAR gene expression and steroidogenesis in mouse Leydig cells.”

     

    Apigenin as an Anti-Aging Skin Treatment

    Skin aging is a complex biological process prematurely induced by innate and external factors. We evaluated the anti-aging effects of apigenin, a plant flavone, on human skin exposed to ultraviolet radiation. A total of 25 female subjects applied a 10% apigenin- containing regimen (eye cream, moisturizer, and serum) to the skin of their faces for eight weeks (56 days), twice daily, once in the morning and once in the evening. At day 28 (the four-week mark) and day 56 (the eight-week mark), we analyzed the treated areas for dermal density, skin elasticity; the length and area of crow’s feet; transepidermal water loss; facial and skin tone evenness; brightness; moisture retention/hydration; the size, depth, and number of wrinkles; roughness; skin hydration; and barrier function. We also evaluated the subjects’ perception and tolerance of the cream. The test regimen was well-tolerated by the study participants for various subjective parameters, including sensory attributes and improvement of overall skin conditions. The anti-aging regimen did not affect the skin barrier function and maintained baseline hydration. The test treatment provided statistically significant improvements in skin roughness and the depth of fine lines and wrinkles for fine wrinkles after 28 days of treatment. Furthermore, significant improvements were measured in skin elasticity for the firmness, maximal amplitude, and extensibility parameters after 56 days of treatment. The anti-aging regimen had a significant effect on skin elasticity. Patient perception of the apigenin containing regimen was excellent. Our findings support the evidence that apigenin can improve several markers of aging. Apigenin use in skin care products may contribute to objectively improved parameters of skin health and subjective appearance of photo-aged skin.

    https://www.sciforschenonline.org/journals/clinical-cosmetic-dermatology/article-data/JCCD-2-128/JCCD-2-128.pdf

    Best taken internally

     

     

    Apigenin has been demonstrated to have VERY POWERFUL anti anxiety, anti depressive, anti Alzheimer’s and anti-excitotoxic neuroprotective capabilities

    What is EXCITOTOXICITY? 

    “Excitotoxicity is the pathological process by which nerve cells are damaged or killed by excessive stimulation by neurotransmitters such as glutamate and similar substances. This occurs when receptors for the excitatory neurotransmitter glutamate (glutamate receptors) such as the NMDA receptor and AMPA receptor are overactivated by glutamatergic storm. Excitotoxins like NMDA and kainic acid which bind to these receptors, as well as pathologically high levels of glutamate, can cause excitotoxicity by allowing high levels of calcium ions (Ca2+) to enter the cell.[1][2] Ca2+ influx into cells activates a number of enzymes, including phospholipases, endonucleases, and proteases such as calpain. These enzymes go on to damage cell structures such as components of the cytoskeleton, membrane, and DNA.

    Excitotoxicity may be involved in spinal cord injury, stroke, traumatic brain injury, hearing loss (through noise overexposure or ototoxicity), and in neurodegenerative diseases of the central nervous system (CNS) such as multiple sclerosis, Alzheimer’s disease, amyotrophic lateral sclerosis (ALS), Parkinson’s disease, alcoholism or alcohol withdrawal and especially over-rapid benzodiazepine withdrawal, and also Huntington’s disease.[3][4] Other common conditions that cause excessive glutamate concentrations around neurons are hypoglycemia.”

     

    Apigenin modulates GABAergic and glutamatergic transmission in cultured cortical neurons

    “Using the patch-clamp technique, we studied the modulation of ionotropic γ-aminobutyric acid (GABA) and glutamate neurotransmission by apigenin, a flavonoid with sedative and antidepressant activity. Apigenin reversibly reduced GABA-evoked currents mediated by α1β2γ2 receptors expressed in HEK293 cells. Amplitude and frequency of spontaneous postsynaptic inhibitory currents (sIPSCs) mediated by GABAA receptors were also decreased by apigenin in cultured cortical neurons. The flavonoid was almost inactive on α-amino-3-hydroxy-5-methylisoxazolepropionic acid (AMPA) mediated currents while it reduced N-methyl-d-aspartate (NMDA) receptor mediated responses with a half maximal inhibiting concentration (IC50) of 10 μM. The flavonoid inhibited also peak amplitude and frequency of spontaneous postsynaptic excitatory currents(sEPSCs). Finally, apigenin is neuroprotective against glutamate-induced neurotoxicity in cerebellar and cortical neurons in culture. Our data reveal the antagonistic effect of apigenin on GABA and NMDAchannels. While the inhibition on GABA receptorcannot explain the effects of the drug in vivo our data on NMDA channels reveal a new target of apigenin. A reduction of the network excitability could thus account for the sedative effects. Furthermore, our data suggest a potential neuroprotective activity of apigenin.”

    Antidepressant-like behavioral and neurochemical effects of the citrus-associated chemical apigenin

    “Apigenin is one type of bioflavonoid widely found in citrus fruits, which possesses a variety of pharmacological actions on the central nervous system. A previous study showed that acute intraperitoneal administration of apigenin had antidepressant-like effects in the forced swimming test (FST) in ddY mice. To better understand its pharmacological activity, we investigated the behavioral effects of chronic oral apigenin treatment in the FST in male ICR mice and male Wistar rats exposed to chronic mild stress (CMS). The effects of apigenin on central monoaminergic neurotransmitter systems, the hypothalamic–pituitary–adrenal (HPA) axis and platelet adenylyl cyclase activity were simultaneously examined in the CMS rats. Apigenin reduced immobility time in the mouse FST and reversed CMS-induced decrease in sucrose intake of rats. Apigenin also attenuated CMS-induced alterations in serotonin (5-HT), its metabolite 5-hydroxyindoleacetic acid (5-HIAA), dopamine (DA) levels and 5-HIAA/5-HT ratio in distinct rat brain regions. Moreover, apigenin reversed CMS-induced elevation in serum corticosterone concentrations and reduction in platelet adenylyl cyclase activity in rats. These results suggest that the antidepressant-like actions of oral apigenin treatment could be related to a combination of multiple biochemical effects, and might help to elucidate its mechanisms of action that are involved in normalization of stress-induced changes in brain monoamine levels, the HPA axis, and the platelet adenylyl cyclase activity.”

     

     

    The Flavonoid Apigenin Protects Brain Neurovascular Coupling against Amyloid-β25-35-Induced Toxicity in Mice

    “Apigenin, one of the most common flavonoids, has demonstrated anti-inflammatory, anticarcinogenic, and free radical-scavenging activities. Recent studies revealed its protective effects against amyloid-β (Aβ)-induced neurotoxicity, but the mechanism was unclear. In the present study, we aimed to explore the anti-amnesic and protective effects of apigenin against Aβ25-35-induced toxicity and the underlying mechanisms in the cerebral cortex in mice. The learning and memory impairments, changes in morphology of major components of neurovascular unit, ultrastructural changes and oxidative stress of cerebral cortex, cerebrovascular dysfunction, and neuronal changes were detected after oral administration of apigenin continuously for 8 days. Our results demonstrate that oral administration of apigenin for Aβ25-35-induced amnesic mice conferred robust neurovascular coupling protection, involving improvement of the learning and memory capabilities, maintenance of neurovascular unit integrity, modulation of microvascular function, reduction of neurovascular oxidative damage, increase of regional cerebral blood flow, improvement of cholinergic system involving the inhibition of AChE activity and elevation of ACh level, and modification of BNDF, TrkB, and phospho-CREB levels.”

     

    In the present study, apigenin inhibited the glutamate-induced [Ca2+]i increase by inhibiting AMPA-, NMDA-, and depolarization-induced Ca2+ influx. Apigenin also inhibited the metabotropic glutamate receptor-induced [Ca2+]i increase and Ca2+-induced Ca2+ release from intracellular stores. These data suggest a possibility that apigenin inhibits synaptic transmission. Reducing [Mg2+]o bathing cultured CNS neurons elicits [Ca2+]i spikes that depends upon glutaminergic synaptic transmission (Rose et al, 1990; Shen et al, 1996; Abel et al, 2000). In this study, apigenin inhibited the synaptically mediated low [Mg2+]o-induced [Ca2+]i spikes. These data suggest that apigenin inhibits glutamatergic synaptic transmission in cultured rat hippocampal neurons by inhibiting AMPA-, NMDA-, and depolarization-induced Ca2+ influx as well as metabotropic glutamate receptor-induced release of Ca2+ from IP3-sensitive intracellular stores and Ca2+-induced Ca2+ release from ryanodine-sensitive stores. However, it has not been studied in the present study whether apigenin affects the release of glutamate in the presynaptic sites, although apigenin inhibited the high K+-induced [Ca2+]i increase in the soma.

    Apigenin has neuroprotective effects against oxidative stress-induced cell death in SH-SY5Y cells (Wang et al, 2001), or glutamate-induced neurotoxicity in cultured cortical neurons (Losi et al, 2004). Our results showed that apigenin inhibits glutamate-induced calcium signaling. These results suggest a possibility that inhibitory effects of apigenin on glutamate-induced calcium signaling can partly be due to the neuroprotection against neuronal cell death, demonstrating a possibility that apigenin might be used as a neuroprotective agent against glutamate-induced neurotoxicity, partly through inhibition of calcium signaling.

     

    Protection of apigenin against excitotoxicity by anti-oxidative effects.

    Apigenin (5,7,4′-trihydroxyflavone) is a principal ingredient of Cirsium japonicum. These experiments were performed to determine whether apigenin has neuroprotective effects against kainic acid (KA)-induced excitotoxicity in vitro and in vivo. Intraperitoneal (i.p.) administration of apigenin (25, 50 mg/kg) decreased the seizure scores induced by KA injection (40 mg/kg, i.p.) in mice. In addition, the convulsion onset time was significantly delayed by apigenin administration. Moreover, we found that apigenin blocked KA-induced seizure-form electroencephalogram (EEG) discharge activity in the brain cortex. In hippocampal cells, apigenin inhibited KA-induced excitotoxicity in a dose-dependent manner as measured by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. To study the possible mechanisms underlying the in vitro neuroprotective effects of apigenin against KA-induced cytotoxicity, we also examined the effect of apigenin on intracellular reactive oxygen species (ROS) elevations in cultured hippocampal neurons and found that apigenin treatment dose-dependently inhibited intracellular ROS elevation. The remarkable reduction of glutathione (GSH) levels induced by KA in hippocampal tissues was reversed by apigenin in a dose-dependent manner. In addition, similar results were obtained after pretreatment with free radical scavengers such as trolox and dimethylthiourea (DMTU). Finally, after confirming the protective effect of apigenin in hippocampal CA3 region, we found apigenin is an active compound in KA-induced neuroprotection. These results collectively indicate that apigenin alleviates KA-induced excitotoxicity by quenching ROS as well as inhibiting GSH depletion in hippocampal neurons.

     

    Neuroprotective effects of apigenin against inflammation, neuronal excitability and apoptosis in an induced pluripotent stem cell model of Alzheimer’s disease.
    “Alzheimer’s disease (AD) is one of the most prevalent neurodegenerative diseases, yet current therapeutic treatments are inadequate due to a complex disease pathogenesis. The plant polyphenol apigenin has been shown to have anti-inflammatory and neuroprotective properties in a number of cell and animal models; however a comprehensive assessment has not been performed in a human model of AD. Here we have used a human induced pluripotent stem cell (iPSC) model of familial and sporadic AD, in addition to healthy controls, to assess the neuroprotective activity of apigenin. The iPSC-derived AD neurons demonstrated a hyper-excitable calcium signalling phenotype, elevated levels of nitrite, increased cytotoxicity and apoptosis, reduced neurite length and increased susceptibility to inflammatory stress challenge from activated murine microglia, in comparison to control neurons. We identified that apigenin has potent anti-inflammatory properties with the ability to protect neurites and cell viability by promoting a global down-regulation of cytokine and nitric oxide (NO) release in inflammatory cells. In addition, we show that apigenin is able to protect iPSC-derived AD neurons via multiple means by reducing the frequency of spontaneous Ca(2+) signals and significantly reducing caspase-3/7 mediated apoptosis. These data demonstrate the broad neuroprotective action of apigenin against AD pathogenesis in a human disease model.”

     

    Apigenin: A Promising Molecule for Cancer Prevention

    “Apigenin, a naturally occurring plant flavone, abundantly present in common fruits and vegetables is recognized as a bioactive flavonoid shown to possess anti-inflammatory, antioxidant and anticancer properties. Epidemiologic studies suggest that a diet rich in flavones is related to a decreased risk of certain cancers, particularly cancers of the breast, digestive tract, skin, prostate and certain hematological malignancies. It has been suggested that apigenin may be protective in other diseases that are affected by oxidative process such as cardiovascular and neurological disorders, although more research needs to be conducted in this regard. Human clinical trials examining the effect of supplementation of apigenin on disease prevention have not been conducted although there is considerable potential for apigenin to be developed as a cancer chemopreventive agent.”

     

    APIGENIN STIMULATES HAIR GROWTH through downregulation of the TGF-β1 gen

    “Androgen-inducible transforming growth factor β (TGF-β1) derived from dermal papilla cells (DPCs) is a catagen inducer that mediates hair growth suppression in androgenetic alopecia (AGA). In this study, a cell-based assay system was developed to monitor TGF-β1 promoter activity and then used to evaluate the effects of activated TGF-β1 promoter in human epidermal keratinocytes (HaCaT). To accomplish this, a pMetLuc-TGF-β1 promoter plasmid that expresses the luciferase reporter gene in response to TGF-β1 promoter activity was constructed. Treatment of HaCaT with dihydrotestosterone, which is known to be a primary factor of AGA, resulted in a concentration-dependent increase in TGF-β1 promoter activity. However, treatment of HaCaT with the TGF-β1 inhibitor, curcumin, resulted in a concentration-dependant decrease in TGF-β1 expression. Subsequent use of this assay system to screen TGF-β1 revealed that HaCaT that were treated with apigenin showed decreased levels of TGF-β1 expression. In addition, treatment with apigenin also significantly increased the proliferation of both SV40T-DPCs (human DPCs) and HaCaT cells. Furthermore, apigenin stimulated the elongation of hair follicles in a rat vibrissa hair follicle organ culture. Taken together, these findings suggest that apigenin, which is known to have antioxidant, anti-inflammatory, and anti-tumor properties, stimulates hair growth through downregulation of the TGF-β1 gene.”

     

    * LONG HALF LIFE; builds up over time. “Blood kinetics showed a high elimination half-time (91.8 hr), a distribution volume of 259 mL, and a plasmatic clearance of 1.95 mL/hr. All of the parameters calculated from these experiments suggested a slow metabolism of apigenin, with a slow absorption and a slow elimination phase. Thus, a possible accumulation of this flavonoid in the body can be hypothesized.”https://www.sciencedirect.com/science/article/pii/S0955286310000379

     

    200 MORE SCIENTIFIC STUDIES ON APIGENIN

    1. Effect of apigenin, kaempferol and resveratrol on the expression of interleukin-1beta and tumor necrosis factor-alpha genes in J774. 2 macrophages.
    2. Topical apigenin improves epidermal permeability barrier homoeostasis in normal murine skin by divergent mechanisms
    3. Apigenin and cancer chemoprevention: progress, potential and promise
    4. An increase in the luteolin: apigenin ratio in Marchantia polymorpha on UV-B enhancement
    5. Anti-inflammatory effects of apigenin on nicotine-and lipopolysaccharide-stimulated human periodontal ligament cells via heme oxygenase-1
    6. Metabolism of apigenin by rat liver phase I and phase II enzymes and by isolated perfused rat liver
    7. Apigenin: a promising molecule for cancer prevention
    8. Dietary apigenin reduces LPS‐induced expression of miR‐155 restoring immune balance during inflammation
    9. The Immune-modulatory and Anti-carcinogenic Mechanisms of the Flavonoid Apigenin
    10. Molecular basis for the action of a dietary flavonoid revealed by the comprehensive identification of apigenin human targets
    11. Inhibition of proteasome activity by the dietary flavonoid apigenin is associated with growth inhibition in cultured breast cancer cells and xenografts
    12. Apigenin inhibits VEGF and HIF-1 expression via PI3K/AKT/p70S6K1 and HDM2/p53 pathways
    13. Apigenin inhibits TGF-β1 induced fibroblast-to-myofibroblast transition in human lung fibroblast populations
    14. Metabolism of flavonoids via enteric recycling: mechanistic studies of disposition of apigenin in the Caco-2 cell culture model
    15. Apigenin inhibits the self-renewal capacity of human ovarian cancer SKOV3‑derived sphere-forming cells
    16. Potential synergy of phytochemicals in cancer prevention: mechanism of action
    17. Enhanced anti-tumor effect of combination therapy with gemcitabine and apigenin in pancreatic cancer
    18. Apigenin and its impact on gastrointestinal cancers
    19. Targeting the PI3K/Akt/mTOR axis by apigenin for cancer prevention
    20. Apigenin inhibits antiestrogen-resistant breast cancer cell growth through estrogen receptor-α-dependent and estrogen receptor-α-independent mechanisms
    21. Apigenin suppresses cancer cell growth through ERβ
    22. Apigenin induces apoptosis via extrinsic pathway, inducing p53 and inhibiting STAT3 and NFκB signaling in HER2-overexpressing breast cancer cells
    23. Protoapigenone, a natural derivative of apigenin, induces mitogen-activated protein kinase-dependent apoptosis in human breast cancer cells
    24. Autophagy inhibition enhances apigenin-induced apoptosis in human breast cancer cells
    25. Apigenin, a dietary flavonoid, inhibits proliferation of human bladder cancer T-24 cells via blocking cell cycle progression and inducing apoptosis
    26. Phytoestrogens: potential benefits and implications for breast cancer survivors
    27. Plant-derived flavone Apigenin: the small-molecule with promising activity against therapeutically resistant prostate cancer
    28. Apigenin and breast cancers: from chemistry to medicine
    29. Flavonoid apigenin modified gene expression associated with inflammation and cancer and induced apoptosis in human pancreatic cancer cells
    30. Role of apigenin in cancer prevention via the induction of apoptosis and autophagy
    31. Combined with Apigenin Synergistically Induced Apoptosis and Inhibited Migration in Human Breast and Liver Cancer
    32. Apigenin and cancer chemoprevention
    33. Protective effect of apigenin on radiation-induced chromosomal damage in human lymphocytes
    34. Suppression of rat and human androgen biosynthetic enzymes by apigenin: possible use for the treatment of prostate cancer
    35. Resveratrol, piperine and apigenin differ in their NADPH-oxidase inhibitory and reactive oxygen species-scavenging properties
    36. Apigenin augments the growth inhibitory effects of doxorubicin in breast cancer cells derived from African American patients
    37. Additive and synergistic effect of phytochemicals in prevention of oral cancer
    38. Oxidative stress triggered by Apigenin induces apoptosis in a comprehensive panel of human cervical cancer-derived cell lines
    39. Modulation of thyroidal radioiodide uptake by oncological pipeline inhibitors and Apigenin
    40. Effect of dietary apigenin on colonic ornithine decarboxylase activity, aberrant crypt foci formation, and tumorigenesis in different experimental models
    41. Dietary apigenin potentiates the inhibitory effect of interferon-α on cancer cell viability through inhibition of 26S proteasome-mediated interferon receptor
    42. Anti-mutagenic and pro-apoptotic effects of apigenin on human chronic lymphocytic leukemia cells
    43. Apigenin inhibits pancreatic cancer cell proliferation through G2/M cell cycle arrest
    44. Bioinformatics and in vitro experimental analyses identify the selective therapeutic potential of interferon gamma and apigenin against cervical squamous cell
    45. Inhibition of mTOR by apigenin in UVB-irradiated keratinocytes: A new implication of skin cancer prevention
    46. Apigenin for chemoprevention, and chemotherapy combined with therapeutic reagents
    47. Apigenin and naringenin suppress colon carcinogenesis through the aberrant crypt stage in azoxymethane-treated rats
    48. Chlorpromazine and apigenin reduce adenovirus replication and decrease replication associated toxicity
    49. Apigenin inhibits HeLa sphere‑forming cells through inactivation of casein kinase 2α
    50. Synthesis, characterization and free radical scavenging activity of apigenin with or without magnesium (II)
    51. Actions of the Dietary Flavone Apigenin in the Context of Human Colorectal Cancer
    52. INHIBITORY EFFECTS OF APIGENIN ON MAMMALIAN DNAPOLYMERASE AND PROLIFERATION OF HUMAN CANCER CELLS
    53. Apigenin stabilized gold nanoparticles increased radiation therapy efficiency in lung cancer cells
    54. ROLE OF APIGENIN IN CANCER PREVENTION
    55. The Flavonoid Apigenin Inhibits Inducible Programmed Death Ligand 1 Expression by Breast Cancer Cells
    56. Apigenin-ask a busy flavone!
    57. The flavonoids apigenin and luteolin suppress ultraviolet A-induced matrix metalloproteinase-1 expression via MAPKs and AP-1-dependent signaling in HaCaT cells
    58. Citrus flavonoids luteolin, apigenin, and quercetin inhibit glycogen synthase kinase-3β enzymatic activity by lowering the interaction energy within the binding cavity
    59. Apigenin: chemopreventive and chemotherapeutic potential for progestin-dependent breast cancer
    60. Degradable poly (apigenin) polymer inhibits tumor cell adhesion to vascular endothelial cells
    61. Apigenin in combination with Akt inhibition significantly enhances thyrotropin-stimulated radioiodide accumulation in thyroid cells
    62. Effects of apigenin, lycopene and astaxanthin on 7β-hydroxycholesterol-induced apoptosis and Akt phosphorylation in U937 cells
    63. Apigenin inhibition of involucrin gene expression is associated with a specific reduction in phosphorylation of PKCδ-Y311
    64. Apigenin prevents development of medroxyprogesterone acetate-accelerated 7, 12-dimethylbenz (a) anthracene-induced mammary tumors in Sprague-Dawley rats
    65. The dietary flavones apigenin and luteolin impair smooth muscle cell migration and VEGF expression through inhibition of PDGFR-β phosphorylation
    66. The natural flavonoid apigenin suppresses Th1-and Th2-related chemokine production by human monocyte THP-1 cells through mitogen-activated protein kinase
    67. Apigenin (4 ‘, 5, 7‐trihydroxyflavone) regulates hyperglycaemia, thyroid dysfunction and lipid peroxidation in alloxan‐induced diabetic mice
    68. The role of apigenin in an experimental model of acute pancreatitis
    69. Protection by chrysin, apigenin, and luteolin against oxidative stress is mediated by the Nrf2-dependent up-regulation of heme oxygenase 1 and glutamate cysteine
    70. Specific role of oxidized species in the bioactivity of two antioxidants: apigenin and 20-hydroxyecdysone
    71. Curcumin and Apigenin–novel and promising therapeutics against chronic neuroinflammation in Alzheimer’s disease
    72. Mechanism of apoptosis induced by apigenin in HepG2 human hepatoma cells: involvement of reactive oxygen species generated by NADPH oxidase
    73. Apigenin: The Anxiolytic Constituent of Turnera aphrodisiaca.
    74. Anti-inflammatory effect of apigenin-7-neohesperidoside (rhoifolin) in carrageenin-induced rat oedema model
    75. Apigenin inhibits TGF-β1-induced proliferation and migration of airway smooth muscle cells
    76. Effects of the vegetable polyphenols epigallocatechin-3-gallate, luteolin, apigenin, myricetin, quercetin, and cyanidin in primary cultures of human retinal
    77. Evaluation of hepatic clearance and drug-drug interactions of luteolin and apigenin by using primary cultured rat hepatocytes
    78. Pharmacokinetic study of luteolin, apigenin, chrysoeriol and diosmetin after oral administration of Flos Chrysanthemi extract in rats
    79. DNA adducts with antioxidant flavonoids: morin, apigenin, and naringin
    80. Apigenin attenuates neointima formation via suppression of vascular smooth muscle cell phenotypic transformation
    81. Neuroprotective and neurotrophic effects of Apigenin and Luteolin in MPTP induced parkinsonism in mice
    82. Preparation of apigenin nanocrystals using supercritical antisolvent process for dissolution and bioavailability enhancement
    83. Apigenin as neuroprotective agent: Of mice and men
    84. The estrogenic effects of apigenin, phloretin and myricetin based on uterotrophic assay in immature Wistar albino rats
    85. Apigenin inhibits C5a-induced proliferation of human nasopharyngeal carcinoma cells through down-regulation of C5aR
    86. Antiadipogenic effect of dietary apigenin through activation of AMPK in 3T3-L1 cells
    87. Apigenin in the regulation of cholesterol metabolism and protection of blood vessels
    88. Efflux transport of chrysin and apigenin sulfates in HEK293 cells overexpressing SULT1A3: The role of multidrug resistance-associated protein 4 (MRP4/ABCC4)
    89. Apigenin inhibits platelet adhesion and thrombus formation and synergizes with aspirin in the suppression of the arachidonic acid pathway
    90. Synergistic activity and mechanism of action of ceftazidime and apigenin combination against ceftazidime-resistant Enterobacter cloacae
    91. Inhibition of superoxide anion-mediated impairment of endothelium by treatment with luteolin and apigenin in rat mesenteric artery
    92. Plant flavone apigenin binds to nucleic acid bases and reduces oxidative DNA damage in prostate epithelial cells
    93. Anti-mutagenic and pro-apoptotic effects of apigenin on human chronic lymphocytic leukemia cells
    94. Enhanced action of apigenin and naringenin combination on estrogen receptor activation in non-malignant colonocytes
    95. Recovery of chicken growth plate by heat-shock protein 90 inhibitors epigallocatechin-3-gallate and apigenin in thiram-induced tibial dyschondroplasia
    96. Neuroprotective effects of apigenin against inflammation, neuronal excitability and apoptosis in an induced pluripotent stem cell model of Alzheimer’s disease
    97. Effects of friedelin on the intestinal permeability and bioavailability of apigenin
    98. Microencapsulation of plant extracts rich in apigenin to be used as chemopreventive agents in functional foods
    99. 5‐Fluorouracil combined with apigenin enhances anticancer activity through mitochondrial membrane potential (ΔΨm)‐mediated apoptosis in hepatocellular
    100. Calcium-and phosphatidylinositol 3-kinase/Akt-dependent activation of endothelial nitric oxide synthase by apigenin
    101. Flavonoid apigenin is an inhibitor of the NAD+ ase CD38: implications for cellular NAD+ metabolism, protein acetylation, and treatment of metabolic syndrome
    102. APIGENIN CAUSES BIOCHEMICAL MODULATION, GLUT4 AND CD38 ALTERATIONS TO IMPROVE DIABETES AND  TO PROTECT DAMAGES OF SOME VITAL ORGANS IN  EXPERIMENTAL DIABETES
    103. Inhibition of CK2α and PI3K/Akt synergistically induces apoptosis of CD34+ CD38− leukaemia cells while sparing haematopoietic stem cells
    104. Flavonoid Apigenin Is an Inhibitor of the NAD+ ase CD38: Implications for Cellular NAD+ Metabolism, Protein Acetylation, and Treatment of Metabolic Syndrome
    105. Dysregulation of the Nadase CD38 impairs articular chondrocyte homeostasis
    106. Role of CD38 expression in diagnosis and pathogenesis of chronic lymphocytic leukemia and its potential as therapeutic target
    107. Effects of apigenin on steroidogenesis and steroidogenic acute regulatory gene expression in mouse Leydig cells
    108. The Roles of Apigenin on Leydig Cells in Testes of Rats [J]
    109. Investigation of testosterone, androstenone, and estradiol metabolism in HepG2 cells and primary culture pig hepatocytes and their effects on 17βHSD7 gene
    110. Effects of apigenin on scrotal heat-induced damage in the mice testis
    111. Natural Compounds to Counteract Testosterone Depletion in Aging
    112. Apigenin inhibits rat neurosteroidogenic 5α-reductase 1 and 3α-hydroxysteroid dehydrogenase
    113. The Pharmacokinetics of Raloxifene and Its Interaction with Apigenin in Rat
    114. Dietary supplements of soya flour lower serum testosterone concentrations and improve markers of oxidative stress in men
    115. Apigenin induces apoptosis through proteasomal degradation of HER2/neu in HER2/neu-overexpressing breast cancer cells via the phosphatidylinositol 3-kinase/Akt
    116. Signal pathways involved in apigenin inhibition of growth and induction of apoptosis of human anaplastic thyroid cancer cells (ARO)
    117. Suppression of protein kinase C and nuclear oncogene expression as possible molecular mechanisms of cancer chemoprevention by apigenin and curcumin
    118. Apigenin inhibits expression of vascular endothelial growth factor and angiogenesis in human lung cancer cells: implication of chemoprevention of lung cancer
    119. Apigenin-induced cell cycle arrest is mediated by modulation of MAPK, PI3K-Akt, and loss of cyclin D1 associated retinoblastoma dephosphorylation in human
    120. Apigenin inhibits HGF-promoted invasive growth and metastasis involving blocking PI3K/Akt pathway and β4 integrin function in MDA-MB-231 breast cancer cells
    121. Stimulatory effect of genistein and apigenin on the growth of breast cancer cells correlates with their ability to activate ER alpha
    122. Degradation of HER2/neu by apigenin induces apoptosis through cytochrome c release and caspase‐3 activation in HER2/neu‐overexpressing breast cancer cells
    123. Activation of PPARγ by a natural flavonoid modulator, apigenin ameliorates obesity-related inflammation via regulation of macrophage polarization
    124. Apigenin ameliorates dyslipidemia, hepatic steatosis and insulin resistance by modulating metabolic and transcriptional profiles in the liver of high-fat diet
    125. Apigenin isolated from Daphne genkwa Siebold et Zucc. inhibits 3T3-L1 preadipocyte differentiation through a modulation of mitotic clonal expansion
    126. Apigenin isolated from the seeds of Perilla frutescens britton var crispa (Benth.) inhibits food intake in C57BL/6J mice
    127. Synergistic interactions of apigenin, naringin, quercetin and emodin on inhibition of 3T3-L1 preadipocyte differentiation and pancreas lipase activity
    128. Apigenin and quercetin ameliorate mitochondrial alterations by tunicamycin-induced ER stress in 3T3-L1 adipocytes
    129. Apigenin, a modulator of PPARγ, attenuates HFD-induced NAFLD by regulating hepatocyte lipid metabolism and oxidative stress via Nrf2 activation
    130. Flavonoids apigenin and quercetin inhibit melanoma growth and metastatic potential
    131. Inhibitory activity of phenolic compounds from extra virgin olive oils on the enzymes involved in diabetes, obesity and hypertension
    132. Studies on mechanistic role of natural bioactive compounds in the management of obesity an overview
    133. The flavonoid compound apigenin prevents colonic inflammation and motor dysfunctions associated with high fat diet-induced obesity
    134. Comparative study of the binding of 3 flavonoids to the fat mass and obesity‐associated protein by spectroscopy and molecular modeling
    135. Effect of Apigenin on the Proliferation and Differentiation of 3T3-L1 Preadipocytes [J]
    136. Phenolic compounds apigenin, hesperidin and kaempferol reduce in vitro lipid accumulation in human adipocytes
    137. Apigenin attenuates diabetes-associated cognitive decline in rats via suppressing oxidative stress and nitric oxide synthase pathway
    138. Antioxidant and protective effects of major flavonoids from Teucrium polium on β-cell destruction in a model of streptozotocin-induced diabetes
    139. Apigenin Attenuates 2-Deoxy-D-ribose-Induced Oxidative Cell Damage in HIT-T15 Pancreatic β-Cells
    140. Associations of dietary flavonoids with risk of type 2 diabetes, and markers of insulin resistance and systemic inflammation in women: a prospective study
    141. Apigenin and naringenin regulate glucose and lipid metabolism, and ameliorate vascular dysfunction in type 2 diabetic rats
    142. The protective effect of apigenin on myocardial injury in diabetic rats mediating activation of the PPAR-γ pathway
    143. Mechanism of action of the stimulatory effect of apigenin-6-C-(2 ″-O-α-l-rhamnopyranosyl)-β-l-fucopyranoside on 14C-glucose uptake
    144. The flavones apigenin and luteolin induce FOXO1 translocation but inhibit gluconeogenic and lipogenic gene expression in human cells
    145. Comparative investigation of in vitro biotransformation of 14 components in Ginkgo biloba extract in normal, diabetes and diabetic nephropathy rat intestinal bacteria
    146. Antidiabetic, antihyperlipidemic and antioxidant effects of the flavonoid rich fraction of Pilea microphylla (L.) in high fat diet/streptozotocin-induced diabetes in mice
    147. Stimulatory effect of apigenin-6-C-β-L-fucopyranoside on insulin secretion and glycogen synthesis
    148. Apigenin restores normal vascular reactivity in diabetic rats via protein kinase C inhibition
    149. Apigenin ameliorates streptozotocin-induced diabetic nephropathy in rats via MAPK-NF-κB-TNF-α and TGF-β1-MAPK-fibronectin pathways
    150. Apigenin attenuates streptozotocin-induced pancreatic β cell damage by its protective effects on cellular antioxidant defense
    151. Dietary flavonoid apigenin inhibits high glucose and tumor necrosis factor α-induced adhesion molecule expression in human endothelial cells
    152. Apigenin alleviates STZ-induced diabetic cardiomyopathy
    153. Anti-hyperglycemic action of apigenin-6-C-β-fucopyranoside from Averrhoa carambola
    154. Effects of C-glycosylation on anti-diabetic, anti-Alzheimer’s disease and anti-inflammatory potential of apigenin
    155. A study on the inhibitory potential of DPP-IV enzyme by apigenin through in silico and in vivo approaches
    156. Pancreatic Β-cell protective effect of rutin and apigenin isolated from Teucrium polium
    157. Saturin-effective vegetative remedy in treatment of type 2 diabetes mellitus
    158. Role of various flavonoids: hypotheses on novel approach to treat diabetes
    159. Apigenin: A methanol fraction component of Newbouldia laevis leaf, as a potential antidiabetic agent
    160. Synthesis and α-glucosidase inhibitory activity of chrysin, diosmetin, apigenin, and luteolin derivatives
    161. Synthesis, nitric oxide release, and α-glucosidase inhibition of nitric oxide donating apigenin and chrysin derivatives
    162. Apigenin inhibits mTORC2 through down-regulation of RICTOR expression in colorectal cancer cells
    163. Inhibitory effect of polyphenolic–rich extract from Cola nitida (Kolanut) seed on key enzyme linked to type 2 diabetes
    164. Apigenin and naringenin ameliorate PKCβII-associated endothelial dysfunction via regulating ROS/caspase-3
    165. GW27-e0367 Apigenin attenuates the cardiac remodeling in experimental diabetic cardiomyopathy
    166. 39 Studies on the antidiabetic activity of apigenin in mice with streptozotocin-induced diabetes
    167. Apigenin attenuates diabetes-associated cognitive decline in rats via suppressing oxidative stress, nitric oxide synthase and anti-apoptotic pathway
    168. Anti-degenerative effect of Apigenin, Luteolin and Quercetin on human keratinocyte and chondrocyte cultures: SAR evaluation
    169. Su1790 Apigenin Analogs Effectively Suppress Pancreatic Stellate Cell Proliferation and Induce Apoptosis
    170. Apigenin inhibition on alpha glucosidase in mice intestinal
    171. Apigenin inhibits tumor necrosis factor alpha plus high glucose-induced LOX-1 expression in human endothelial cells
    172. Apigenin induces apoptosis in Hep G2 cells: possible role of TNF-α and IFN-γ
    173. Apigenin: A current review on its beneficial biological activities
    174. Improvement of Anti-Cancer Activity through the Structural Modification of Gamma-Irradiated Apigenin in H1975 Human Non-Small Lung Cell
    175. Flavonoid apigenin inhibits lipopolysaccharide-induced inflammatory response through multiple mechanisms in macrophages
    176. Apigenin inhibits endothelial‐cell proliferation in G2/M phase whereas it stimulates smooth‐muscle cells by inhibiting P21 and P27 expression
    177. Vasodilatory effects of flavonoids in rat aortic smooth muscle. Structure-activity relationships.
    178. Effects of apigenin on the serum-and platelet derived growth factor-BB-induced proliferation of rat aortic vascular smooth muscle cells
    179. Apigenin, a component of Matricaria recutita flowers, is a central benzodiazepine receptors-ligand with anxiolytic effects
    180. Apigenin inhibits cell migration through MAPK pathways in human bladder smooth muscle cells
    181. Endothelium-dependent vasorelaxant and antiproliferative effects of apigenin
    182. Vasodilatory action mechanisms of apigenin isolated from Apium graveolens in rat thoracic aorta
    183. Inhibition of guinea pig intestinal peristalsis by the flavonoids quercetin, naringenin, apigenin and genistein
    184. Apigenin decreases expression of the myofibroblast phenotype
    185. Suppression of inducible cyclooxygenase and inducible nitric oxide synthase by apigenin and related flavonoids in mouse macrophages
    186. Apigenin inhibits tumor angiogenesis through decreasing HIF-1α and VEGF expression
    187. Cytotoxicity of apigenin on leukemia cell lines: implications for prevention and therapy
    188. A cell-based system for screening hair growth-promoting agents
    189. Taken together, these findings suggest that APIGENIN, which is known to have antioxidant, anti-inflammatory, and anti-tumor properties, stimulates hair growth through downregulation of the TGF-beta1 gene.
    190. Effects of seven pure flavonoids from mosses on germination and growth of Tortula muralis HEDW.(Bryophyta) and Raphanus sativus L.(Magnoliophyta)
    191. Apigenin, a chemopreventive bioflavonoid, induces AMP‐activated protein kinase activation in human keratinocytes
    192. Enhancement of p53 expression in keratinocytes by the bioflavonoid apigenin is associated with RNA‐binding protein HuR
    193. The flavone apigenin blocks nuclear translocation of sterol regulatory element-binding protein-2 in the hepatic cells WRL-68
    194. AMPK-mTOR axis as key target for chemoprevention of UV-induced skin cancer by the bioflavonoid apigenin
    195. Apigenin and luteolin display differential hypocholesterolemic mechanisms in mice fed a high-fat diet
    196. Apigenin-7-O-β-d-(-6 ″-p-coumaroyl)-glucopyranoside pretreatment attenuates myocardial ischemia/reperfusion injury via activating AMPK signaling
    197. The flavone apigenin blocks SREBP-2 activation in hepatic cells
    198. Apigenin Ameliorates the Obesity‐Induced Skeletal Muscle Atrophy by Attenuating Mitochondrial Dysfunction in the Muscle of Obese Mice
    199. Apigenin-induced apoptosis is enhanced by inhibition of autophagy formation in HCT116 human colon cancer cells
    200. Reversal of Warburg effect by Apigenin and 5-Fluorouracil loaded dual drug liposomes result in enhanced colorectal chemotherapy

     

    7 reviews for APIGENIN 200:1

    1. Rated 5 out of 5

      CC – August 20, 2018

      Though I have only been taking this for a little while compared to taking the spice and peel for a much longer time. I can tell that my joints feel like they have less inflammation. A few days ago I was in a lot of pain and Gavin told me to take a megadose of spice which I did and then I added a scoop of the apeginin and the pain subsided even more. I was very grateful for the lessened pain. I look forward to seeing how my joints continue to feel.

    2. Rated 5 out of 5

      Stephen – December 31, 2018

      I initially ordered this with Spice/Peel about three months ago to train for a professional event, after asking Gavin for advice on what to take.
      I’ve been training twice a day since then and remarkably my blood tests showed my free testosterone has improved! I’ve struggled with my free testosterone levels for several years now and I’m really amazed this worked.
      I’ve just ordered the 10 spice combo and look forward to taking my training to the next level!

    3. Rated 5 out of 5

      Luz Carter – June 29, 2019

      My latest purchase was Apigenin. I bought this one due to the effect of healing in the liver. I have what’s known as esophageal varices. They were discovered when I was in my mid twenties. I’m not a heavy drinker by any means. From what we can tell it’s due to when I had my spleen removed and apparently an injured portal vein as a premie. I had my gall bladder out shortly after my daughter was born 13 years ago and they nicked one of the varices during that surgery. To this day I still have a blood clot near that area. I’m taking Apigenin as another means to heal my insides. I can tell a difference already. I don’t ache as much in that area anymore and I’m continuing to lose belly fat with dry fasting and the blends. Definitely keeping this one in my arsenal. Gavin, you are the “Master of Herbs” and I’m so glad I placed an order. I am a life long believer in your product and I tell people every day how much these blends have improved my health. Keep doing what you’re doing because you’re changing the lives of MANY!

    4. Rated 5 out of 5

      Rich Ryan – August 21, 2019

      “Wanted to share that I’ve experienced a significant decrease in my heart disease symptoms over the last year since I doubled my Spice/Peel intake. I can tell the main blockage on my Widow Maker artery on the back of my heart, that I’ve been carrying for over 15 years, has shrunk significantly. The proof is that when I have a bad day and eat all kinds of crap that I shouldn’t eat, I experience almost no symptoms from it. A year ago I would’ve almost died from eating all that garbage. Now, almost nothing.
      Also, my depression is pretty much gone since starting Apigenin, Luteolin, and supplementing with Mag, Zinc and Lithium. 1/4 tsp API, 1/2 tsp Lut, 4 caps Mag and Zinc, 10 drops Lithium. Twice a day for all.
      My Spice/Peel intake is 2 tsp 20:1, 1/2 tsp 200:1. I alternate between 20:1 and 200:1. Usually do one of them 20:1 and the other 200:1, and switch it up every month or two. Take one in the morning, the other in the evening.
      So Gavin has hit on the cure for arterial blockages as well. Amazing stuff!”

    5. Rated 5 out of 5

      michael mannino – April 8, 2020

      Apegenin has been a game changer. I have been taking Apegenin for over a year now. I was prescribed Ritalin since the age of 13, I always skipped my doses and denied any of the anti depressants the doctors always offered me. After years of battling with depression from the drugs, I finally rid my body of all these artificial, dangerous, and unhealthy chemicals from my lifestyle. That was a long time ago, and since then I have been always searching for uplifting, health enhancing, anti-aging elements to pair with my diet. I searched for years for ancient herbs, finally I found Gavin through my friends group and thank god for that. I always praise his products because they have given me the chance to challenge myself and have major benefits at the same time. These products may seem like a hefty investment, but what does your health and your life at the very core mean to you? If filling your body with chocolate and soda is your answer, then this probably isn’t for you(and maybe SHOULD BE). If you want to start a new healthy lifestyle, or continue fulfilling your goals and add a powerful, life-changing element into the mix to join you, then what the F&^% are you waiting for? I’m about to get another batch, using these blends are the favorite part of my day and I always look forward to continuing life and smashing the impossible with them by my side. Cheers Gavin, and thank you!!!

    6. Rated 5 out of 5

      Paul Benson (verified owner) – September 29, 2020

      Alright, I’ve got to talk about apigenin for a moment here. I told Gavin some of my issues, and he got back to me (within minutes, the guy’s a beast) with his recommendations. I’ve tried and use a fair amount of the blends, but I hadn’t used apigenin yet. So I gave it try.
      I’m not one to write a review just after a few days of taking a supplement or medicine. I’ve been around long enough and tried enough supplements and medicines that I know I need to use it for at least a month, but preferably, several months before I can give an honest review. And the long and short of it is, after around four months of taking apigenin, I recommend it.
      Now, it took me a bit to figure out the right timing to take apigenin, so I’d encourage you to give it a few days and if you notice anything negative, try what I did first and then see where you are from there. What I learned is that if I took it first thing in the morning and on its own, it gave me a powerful boost for the day, lowered the heart problems I’ve dealt with for years, and gave me a bigger drive (both libido and life, though I think both are highly related).
      I’ll go into a bit more detail here. Because it’s powerful and can increase testosterone, I’ll share a bit of detail that may be too much for some, but something I think every guy should know, and which I’ll get to in a minute. But first, the effects on my heart. I’ve had a condition known as Prinzmetal Angina for the past 18 years (this Oct is the 18th anniversary). Spice was a game-changer, and I truly believe saved my life, but I also wanted to add a bit more because there was a ton of damage done over the years. Spice took the constant pain and the ick feeling away–what Apigenin has done has helped lower the amount of spasms I’ve been experiencing (Prinzmetal, or variant, angina, is where the coronary arteries spasm). What this translates to is more energy and stamina, and less pain and exhaustion overall. When a spasm comes, it can leave me wiped out, so not having as many has been huge.
      Next, I literally started getting more tiny hairs growing on my head. (Makes me think adding in the Hair Tonic would be a good idea!) I’ve said for years that my one vanity is having hair, so when it started thinning that sucked. This has literally been helping restore the hair.
      Now for the “guy” part. If it’s too much info, sorry, but I think it’s important, especially in our time when there are so many estrogen boosters in so many products from medicine to food to even detergents. After about a month of consistent use, I noticed that the boys started feeling heavier. Not much mind you, but a little bit. I wasn’t sure if I was just imagining things, and so I’ve paid close attention. And over the months, they grew. In fact, just from the feel alone, now I’d say they weigh 1.5-2 times more than what they did before. This is no exaggeration. I’m a lot fuller than I’ve ever been down there and now in the bedroom, there’s been a lot less frustration on both mine and my wife’s part. And even though I’ve been getting older, I can perform better now and more often than I could for probably the last six to seven years.
      All in all, I love this product, and I HIGHLY recommend it!

    7. Rated 5 out of 5

      Alecxander Castro – October 14, 2020

      I first heard from Interstellar blends from Shaun Lee on Instagram. I hesitated cuz of the price but after a few months I dove in and got every single product from Gavin to see which one was best for my lifestyle.

      I work in a hedgefund so I need to have my brain on point all the time and I found that my favorite herbs were: Apigenin, Shilajit, Victorious, Peel, Spice, ALZ, Luteolin, Hypnotic to sleep, Super Tonic Hair, and Pine Pollen. I take them pure with hot water.

      I lead a pretty active and healthy lifestyle and I found that combining these blends with my morning green shake of veggies and fruits, my cognitive functions and my brain in general works so much better. It even helps me to meditate more deeply and productively. They will be in my arsenal of tools to boost my brain. The more you use Apigenin, the more brain cells you form in your brain cuz of neuro genesis. How cool is that! If I understand it correctly, you get smarter by every month using it while leading a healthy lifestyle!

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