The underlined effects of diallyl sulfide (DAS) against CCL4 -induced oxidative, inflammatory, and apoptotic acute hepatic damage were assessed. Administration of DAS (50, 100, and 200 mg/kg) along with CCL 4 effectively mitigated serum aspartate aminotransferase, alanine aminotransferase activities, MDA, TNF-α, IL-1β, and MCP-1 levels, as well as significantly restored HO-1, GSH levels and SOD activity in liver tissues compared with those in rats treated with CCL 4 . Moreover, DAS inhibited CCL 4 -induced increase of liver NF-κB (p65), Bax, p38 MAPK, and JNK protein expression. In addition, DAS accelerated protein expression of Nrf2 and Bcl-2. The hepatoprotective properties of DAS were further confirmed by the reduced severity of hepatic damage as demonstrated by histopathological findings. In conclusion, DAS achieved its protective potential against CCL4-induced hepatotoxicity through antiapoptotic activity, as well as the synchronized modulation of NF-κB and Nrf2 for the favor of antioxidant/anti-inflammatory effects via suppression of the upstream stress-activated MAPKs pathways.
Keywords: JNK; carbon tetrachloride (CCl4); diallyl sulfide (DAS); hepatotoxicity; p38 MAPK.
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