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Diallyl sulfide ameliorates carbon tetrachloride‐induced hepatotoxicity in rats via suppressing stress‐activated MAPK signaling pathways
Author(s) -
Elkhoely Abeer
Publication year - 2019
Publication title -
journal of biochemical and molecular toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.526
H-Index - 58
eISSN - 1099-0461
pISSN - 1095-6670
DOI - 10.1002/jbt.22307
Subject(s) - carbon tetrachloride , oxidative stress , chemistry , p38 mitogen activated protein kinases , mapk/erk pathway , ccl4 , pharmacology , antioxidant , apoptosis , glutathione , alanine aminotransferase , signal transduction , biochemistry , endocrinology , enzyme , medicine , organic chemistry
The underlined effects of diallyl sulfide (DAS) against CCL 4 ‐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.