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
  • 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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