Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
8546401 | Food and Chemical Toxicology | 2018 | 10 Pages |
Abstract
The effects of diallyl sulfide (DAS) and the potential mechanisms were investigated on lipopolysaccharide (LPS)/d-galactosamine (D-GalN)-induced acute liver injury in mice. DAS (50, 100, 200â¯Î¼mol/kg) were orally given 1â¯h prior to LPS (10â¯Î¼g/kg)/D-GalN (500â¯mg/kg) intraperitoneal injection. Serum and liver were collected at 8â¯h after LPS/D-GalN treatment. DAS Pretreatment reduced the activities of serum aminotransferase and attenuated histopathological damage in LPS/D-GalN-induced liver injury. Additionally, LPS/D-GalN-induced liver oxidative stress was ameliorated by DAS pretreatment, as evidenced by the decreased content of MDA and increased level of GSH, SOD, CAT in liver. Moreover, LPS/D-GalN-induced the excessive levels of TNF-α, IL-1β and MCP-1 in serum and liver was decreased by DAS pretreatment. Furthermore, DAS pretreatment attenuated LPS/D-GalN-induced hepatocyte apoptosis, as evidenced by TUNEL staining and protein expression of cleaved caspase3, Bax and Bcl-2 in liver. DAS also up-regulated the expression of p-PI3K p85 and p-Akt in a dose-dependent manner, and Akt inhibitor MK-2206 weakened the inhibitory effect of DAS on hepatocyte apoptosis induced by LPS/D-GalN. In conclusion, the results suggest that DAS exerts the protective effect on LPS/GalN-induced acute liver injury, and this effects possibly by suppressing oxidative stress, inflammation and regulating hepatocyte apoptosis via the PI3K/Akt pathway.
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Authors
Ming Li, Shuo Wang, Xianjie Li, Lulu Jiang, Xujing Wang, Ruirui Kou, Qiong Wang, Lin Xu, Ning Zhao, Keqin Xie,