Hepatoprotective - Thymoquinone, the active constituent of Nigella sativa, was tested in isolated rat hepatocytes as a hepatoprotective agent against tert-butyl hydroperoxide (TBHP) toxicity. TBHP (2 mM) was used to produce oxidative injury in isolated rat hepatocytes and caused progressive depletion of intracellular glutathione (GSH), loss of cell viability as evidenced by trypan blue uptake and leakage of cytosolic enzymes, alanine transaminase (ALT) and aspartic transaminase (AST).

Preincubation of hepatocytes with 1 mM of either thymoquinone or silybin, which is a known hepatoprotective agent, resulted in the protection of isolated hepatocytes against TBHP induced toxicity evidenced by decreased leakage of ALT and AST, and by decreased trypan blue uptake in comparison to TBHP treated hepatocytes.

Both thymoquinone and silybin prevented TBHP induced depletion of GSH to the same extent. Although thymoquinone protected the liver enzymes leakage, the degree of protection was less than that caused by silybin.

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Anti-Tumor - The objective of the present study was to evaluate the in vitro and in vivo anti-cancer effect of Nigella sativa L. seed extracts. The essential oil (IC₅₀ = 0.6%, v/v) and ethyl acetate (IC₅₀ = 0.75%) extracts were more cytotoxic against the P815 cell line than the butanol extract (IC₅₀ = 2%).

The present study demonstrates that the cytotoxic activity of blackseed extracts is a complex phenomenon depending not only on the nature of the extract and its components, but also on the tumor cell type. We report here a very high efficacy of the essential oil in reducing tumor volume, inhibiting metastasis development and delaying mortality of P815 tumor-bearing mice.

Additional research is now necessary in order to determine the agents responsible for these in vitro and in vivo anti-cancer activities as well as the molecular mechanisms involved in their effects.

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We demonstrate that the aqueous extract of Nigella sativa significantly enhances splenocyte proliferation in a dose–responsive manner.

Our data present Nigella sativa as a traditionally used herb with potent immunomodulatory, anti-inflammatory, and anti-tumor effects. We anticipate that Nigella sativa ingredients may be employed as effective therapeutic agents in the regulation of diverse immune reactions implicated in various conditions and diseases such as cancer.

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Anti-Cancer - Thymoquinone (TQ) is the bioactive constituent of the volatile oil of black seed. It has been shown to exert anti-neoplastic and anti-inflammatory effects.

TQ is known to induce apoptosis by p53-dependent and p53-independent pathways in cancer cell lines. Growth inhibition is associated with induction of cell cycle arrest.

The combination of TQ with clinically used anti-cancer drugs has led to improvements in their therapeutic index and prevents non-tumor tissues from sustaining chemotherapy-induced damage.

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Anti-Allergy - We investigated whether N. sativa, one of its components, thymoquinone, or synthetic opioid receptor (OR)-agonists can alleviate food allergy.

We demonstrate that N. sativa seed extract significantly improves symptoms and immune parameters in murine OVA-induced allergic diarrhea; this effect is at least partially mediated by thymoquinone. ORs may also be involved and could be a new target for intestinal allergy symptom alleviation.

N. sativa seed extract seems to be a promising candidate for nutritional interventions in humans with food allergy.

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Anticonvulsant - The anticonvulsant effects of thymoquinone, the major constituent of Nigella sativa seeds, were investigated using pentylenetetrazole (PTZ)- and maximal electroshock (MES)-induced seizure models.

These results indicate that thymoquinone may have anticonvulsant activity in the petit mal epilepsy probably through an opioid receptor-mediated increase in GABAergic tone.

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Anti-Inflammatory - We have recently shown that thymoquinone (Tq), the major constituent of Nigella sativa oil extract, induced apoptosis and inhibited proliferation in PDA cells.

In this study, we evaluated the anti‐inflammatory potential of Tq in PDA cells in comparison with that of a specific HDAC inhibitor, trichostatin A (TSA).

Our data demonstrate previously undescribed anti‐inflammatory activities of Tq in PDA cells, which are paralleled by inhibition of NF‐κB. Tq as a novel inhibitor of proinflammatory pathways provides a promising strategy that combines anti‐inflammatory and proapoptotic modes of action.

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