Hepatoprotective effects of salidroside on fulminant hepatic failure induced by D-galactosamine and lipopolysaccharide in mice

被引:0
作者
Wu, Yan-Ling [1 ]
Lian, Li-Hua [1 ]
Jiang, Ying-Zi [1 ]
Nan, Ji-Xing [1 ]
机构
[1] Yanbian Univ, Key Lab Nat Resource Changbai Mt & Funct Mol, Minist Educ, Coll Pharm, Yanji 133002, Jilin Province, Peoples R China
基金
中国国家自然科学基金;
关键词
antioxidation; D-galactosamine; hypoxia-inducible factor-1 alpha; lipopolysaccharide; nitric oxide; salidroside; HYPOXIA-INDUCIBLE FACTOR-1; NITRIC-OXIDE; APOPTOSIS; ENDOTOXIN; HEPATOCYTES; INJURY; CELLS;
D O I
10.1211/jpp/61.10.0015
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Objectives The aim was to investigate the protective effect of salidroside isolated from Rhodiola sachalinensis A. Bor. (Crassulaceae) on D-galactosamine/lipopolysaccharide-induced fulminant hepatic failure. Methods Hepatotoxicity was induced by an intraperitoneal injection Of D-galactosamine (700 mg/kg) and lipopolysaccharide (10 mu g/kg); salidroside (20, 50 and 400 mg/kg) was administered intraperitoneally I h before induction of hepatoxicity. Liver injury was assessed biochemically and histologically. Key findings Salidroside attenuated the induced acute increase in serum aspartate aminotransferase and alanine aminotransferase activities, and levels of tumour necrosis factor-alpha levels and serum nitric oxide. It restored depleted hepatic glutathione, superoxide dismutase, catalase and glutathione peroxidase activities, decreased malondialdehyde levels and considerably reduced histopathological changes. Histopathological, immunohistochemical and Western blot analyses also demonstrated that salidroside could reduce the appearance of necrotic regions and expression of caspase-3 and hypoxia-inducible factor-1 alpha in liver tissue. Conclusions Salidroside protected liver tissue from the oxidative stress elicited by D-galactosamine and lipopolysaccharide. The hepatoprotective mechanism of salidroside appear to be related to antioxidant activity and inhibition of hypoxia-inducible factor-1 alpha.
引用
收藏
页码:1375 / 1382
页数:8
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