Betulin inhibits lipopolysaccharide/D-galactosamine-induced acute liver injury in mice through activating PPAR-γ

被引：17
作者：
Xu Guang-men [1 ]
Zan Tao [2 ]
Li Hong-yan [2 ]
Han Jin-feng [2 ]
Liu Zhong-min [2 ]
Huang Ju [2 ]
Dong Li-hua [2 ]
Zhang Hai-na [3 ]
机构：
[1] Jilin Univ, Hosp 2, Dept Colorectal & Anal Surg, Changchun 130041, Jilin, Peoples R China
[2] Jilin Univ, Hosp 1, Dept Intens Care Unit, Changchun 130021, Jilin, Peoples R China
[3] Jilin Univ, Hosp 2, Dept Rehabil, Changchun 130041, Jilin, Peoples R China
来源：
BIOMEDICINE & PHARMACOTHERAPY | 2018年 / 106卷
关键词：
Betulin; Acute liver injury; Lipopolysaccharide; D-galactosamine; NF-kappa B; KAPPA-B; INFLAMMATORY PATHWAYS; FAILURE; HOMEOSTASIS; APOPTOSIS; PROTECTS; DISEASE; RATS;
D O I：
10.1016/j.biopha.2018.07.011
中图分类号：
R-3 [医学研究方法]; R3 [基础医学];
学科分类号：
1001 ;
摘要：
Betulin is a phenolic flavonoid which has been reported to possess a mass of pharmacological properties, especially anti-inflammatory activity. The purpose of this study was to explore the protective effects and possible mechanism of betulin against lipopolysaccharide/D-galactosamine (LPS/D-Gal)-induced acute liver injury. D-Gal and LPS were intraperitoneally injected to develop acute liver injury animal model. Betulin (2, 4 or 8 mg/kg) were given 1 h before LPS/D-Gal instillation. Liver tissues and plasma samples were collected 9 h after LPS/DGal were given. The results indicated that betulin dramatically decreased liver pathologic changes, myeloperoxidase (MPO) activity, serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels. Simultaneously, the levels of interleukin (IL-1 beta) and tumor necrosis factor (TNF-alpha) in serum and liver tissues were both attenuated by betulin. Besides, betulin suppressed NF-kappa B pathway activation in a dose-dependently manner. Betulin increased the expression of PPAR-gamma in a dose-dependent manner. In conclusion, all these results revealed that betulin could possess potential therapeutic effect for LPS/D-Gal-induced acute liver injury.
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收藏
页码：941 / 945
页数：5
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