标题：Diallyl sulfide protects against lipopolysaccharide/D-galactosamine-induced acute liver injury by inhibiting oxidative stress, inflammation and apoptosis in mice
作者：Li, Ming; Wang, Shuo; Li, Xianjie; Jiang, Lulu; Wang, Xujing; Kou, Ruirui; Wang, Qiong; Xu, Lin; Zhao, Ning; Xie, Keqin
作者机构：[Li, Ming; Li, Xianjie; Jiang, Lulu; Wang, Xujing; Kou, Ruirui; Wang, Qiong; Xu, Lin; Zhao, Ning; Xie, Keqin] Shandong Univ, Sch Publ Hlth, Inst Toxic 更多
通讯作者地址：[Xie, KQ]Shandong Univ, Sch Publ Hlth, Inst Toxicol, Jinan 250012, Shandong, Peoples R China.
来源：FOOD AND CHEMICAL TOXICOLOGY
关键词：Diallyl sulfide; LPS/D-GalN; Acute liver injury; Apoptosis; PI3K/Akt; pathway
摘要：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, 200 mol/kg) were orally given 1 h prior to LPS (10 mu g/kg)/D-GalN (500 mg/kg) intraperitoneal injection. Serum and liver were collected at 8 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-alpha, IL-1 beta 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.