2. Academic Validation
  3. Diallyl sulfide protects against lipopolysaccharide/d-galactosamine-induced acute liver injury by inhibiting oxidative stress, inflammation and apoptosis in mice

Diallyl sulfide protects against lipopolysaccharide/d-galactosamine-induced acute liver injury by inhibiting oxidative stress, inflammation and apoptosis in mice

  • Food Chem Toxicol. 2018 Oct;120:500-509. doi: 10.1016/j.fct.2018.07.053.
Ming Li 1,  Shuo Wang 2,  Xianjie Li 3,  Lulu Jiang 4,  Xujing Wang 5,  Ruirui Kou 6,  Qiong Wang 7,  Lin Xu 8,  Ning Zhao 9,  Keqin Xie 10
Affiliations

Affiliations

  • 1 Institute of Toxicology, School of Public Health, Shandong University, Jinan, Shandong Province, 250012, China. Electronic address: [email protected].
  • 2 School of Pharmaceutical, Liaocheng University, Liaocheng, Shandong Province, 252000, China. Electronic address: [email protected].
  • 3 Institute of Toxicology, School of Public Health, Shandong University, Jinan, Shandong Province, 250012, China. Electronic address: [email protected].
  • 4 Institute of Toxicology, School of Public Health, Shandong University, Jinan, Shandong Province, 250012, China. Electronic address: [email protected].
  • 5 Institute of Toxicology, School of Public Health, Shandong University, Jinan, Shandong Province, 250012, China. Electronic address: [email protected].
  • 6 Institute of Toxicology, School of Public Health, Shandong University, Jinan, Shandong Province, 250012, China. Electronic address: [email protected].
  • 7 Institute of Toxicology, School of Public Health, Shandong University, Jinan, Shandong Province, 250012, China. Electronic address: [email protected].
  • 8 Institute of Toxicology, School of Public Health, Shandong University, Jinan, Shandong Province, 250012, China. Electronic address: [email protected].
  • 9 Institute of Toxicology, School of Public Health, Shandong University, Jinan, Shandong Province, 250012, China. Electronic address: [email protected].
  • 10 Institute of Toxicology, School of Public Health, Shandong University, Jinan, Shandong Province, 250012, China. Electronic address: [email protected].
PMID: 30075314 DOI: 10.1016/j.fct.2018.07.053
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, 200 μmol/kg) were orally given 1 h prior to LPS (10 μg/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-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.

Keywords

Acute liver injury; Apoptosis; Diallyl sulfide; LPS/D-GalN; PI3K/Akt pathway.

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