Thymoquinone therapy remediates elevated brain tissue inflammatory mediators induced by chronic administration of food preservatives.
Ahmed Mohsen Elsaid HamdanMohammed M Al-GayyarMohamed E E ShamsUdai Salamh AlshamanKousalya PrabaharAlaa BagalagelReem DiriAhmad O NoorDiena AlmasriPublished in: Scientific reports (2019)
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.
Keyphrases
- oxidative stress
- resting state
- white matter
- nitric oxide
- diabetic rats
- induced apoptosis
- functional connectivity
- cell death
- cerebral ischemia
- ischemia reperfusion injury
- rheumatoid arthritis
- signaling pathway
- anti inflammatory
- stem cells
- multiple sclerosis
- young adults
- bone marrow
- risk assessment
- immune response
- physical activity
- epithelial mesenchymal transition
- systemic sclerosis
- climate change
- inflammatory response
- fatty acid
- subarachnoid hemorrhage
- idiopathic pulmonary fibrosis
- toll like receptor