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Food Chem Toxicol. 2018 Oct;120:500-509. doi: 10.1016/j.fct.2018.07.053. Epub 2018 Jul 31.

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

Author information

1
Institute of Toxicology, School of Public Health, Shandong University, Jinan, Shandong Province, 250012, China. Electronic address: liming1107@163.com.
2
School of Pharmaceutical, Liaocheng University, Liaocheng, Shandong Province, 252000, China. Electronic address: wangshuo@lcu.edu.cn.
3
Institute of Toxicology, School of Public Health, Shandong University, Jinan, Shandong Province, 250012, China. Electronic address: 1321935119@qq.com.
4
Institute of Toxicology, School of Public Health, Shandong University, Jinan, Shandong Province, 250012, China. Electronic address: jllsdu@163.com.
5
Institute of Toxicology, School of Public Health, Shandong University, Jinan, Shandong Province, 250012, China. Electronic address: 1308642670@qq.com.
6
Institute of Toxicology, School of Public Health, Shandong University, Jinan, Shandong Province, 250012, China. Electronic address: kouruirui@sdu.edu.cn.
7
Institute of Toxicology, School of Public Health, Shandong University, Jinan, Shandong Province, 250012, China. Electronic address: 542777036@qq.com.
8
Institute of Toxicology, School of Public Health, Shandong University, Jinan, Shandong Province, 250012, China. Electronic address: xulin992@163.com.
9
Institute of Toxicology, School of Public Health, Shandong University, Jinan, Shandong Province, 250012, China. Electronic address: 13996420084@163.com.
10
Institute of Toxicology, School of Public Health, Shandong University, Jinan, Shandong Province, 250012, China. Electronic address: keqinx@sdu.edu.cn.

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

PMID:
30075314
DOI:
10.1016/j.fct.2018.07.053
[Indexed for MEDLINE]

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