article · Scientific Reports
Continuous exposure to food preservatives such as nitrite salts can cause harmful effects in various organs. This research evaluated whether thymoquinone, the primary bioactive constituent of Nigella sativa oil, could counter brain damage triggered by sodium nitrite. Male rats received daily doses of sodium nitrite, either alone or alongside thymoquinone. Administering sodium nitrite alone prompted significant brain inflammation, oxidative stress, cellular damage, and apoptosis. Specific changes included elevated inflammatory cytokines, malondialdehyde, fibrotic factors, and apoptotic markers, alongside depleted antioxidants, cytochrome c oxidase, and protective signalling factors. Co-administration of thymoquinone effectively mitigated these harmful shifts. It restored antioxidant levels, blocked inflammatory markers, revived enzyme function, and lowered indicators of programmed cell death in brain tissue.
Common food preservatives such as nitrite salts pose potential risks to neurological health through prolonged exposure. Identifying natural compounds that reduce these toxic effects offers insights into protective therapies. This study highlights how a compound derived from Nigella sativa oil counters chemical-induced brain damage, suggesting mechanisms to protect brain tissues against oxidative injury, inflammation, and cellular death.
The findings point towards potential therapeutic or dietary supplement formulations using thymoquinone to protect neurological tissues from preservative-induced toxicity. Likely users would be pharmaceutical or nutraceutical product developers investigating protective agents. However, as this investigation is early-stage animal research conducted in rats, significant translational work, formulation development, and clinical evaluation in humans are required before any practical application can be realised.
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Continuous exposure to preservatives such as nitrite salts has deleterious effects on different organs. Meanwhile, Nigella sativa oil can remediate such organ dysfunction. Here, we studied the effect of consumption of thymoquinone (TQ); the main component of Nigella sativa oil on the brain damage induced by sodium nitrite. Forty adult male rats were daily given oral gavage of sodium nitrite (80 mg/kg) with or without thymoquinone (50 mg/kg). Oxidative stress, cytokines of inflammation, fibrotic elements and apoptotic markers in brain tissue were measured. Exposure to sodium nitrite (SN) resulted in increased levels of malondialdehyde, TGF-β, c-reactive protein, NF-κB, TNF-α, IL-1β and caspase-3 associated with reduced levels of glutathione, cytochrome c oxidase, Nrf2 and IL-10. However, exposure of rats' brain tissues to thymoquinone resulted ameliorated all these effects. In conclusion, thymoquinone remediates sodium nitrite-induced brain impairment through several mechanisms including attenuation of oxidative stress, retrieving the reduced concentration of glutathione, blocks elevated levels of pro-inflammatory cytokines, restores cytochrome c oxidase activity, and reducing the apoptosis markers in the brain tissues of rats.
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DOI: 10.1038/s41598-019-43568-x
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