γ-Aminobutyric Acid B Receptor Improves Carbon Tetrachloride-Induced Liver Fibrosis in Rats

被引:10
作者
Fan, Wenmei [1 ]
Shi, Bingyi [1 ]
Wei, Hongshan [2 ]
Ma, Xihui [1 ]
He, Xiuyun [1 ]
Feng, Kai [1 ]
机构
[1] Chinese Peoples Liberat Army, Hosp 309, Inst Organ Transplantat, Beijing 100091, Peoples R China
[2] Beijing Ditan Hosp, Inst Infect Dis, Chaoyang Dist 100015, Peoples R China
基金
中国国家自然科学基金;
关键词
Liver fibrosis; GABA-B receptor; Alpha-smooth muscle actin; Carbon tetrachloride; HEPATIC-FIBROSIS; TISSUE DISTRIBUTION; MECHANISMS; INTERFERON; REGRESSION; APOPTOSIS; NEUROLOGY; NEURONS; CLONING;
D O I
10.1007/s10620-013-2623-z
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
It was well known that angiotension II can inhibit hepatic stellate cell activation. The GABA(B) receptor was upregulated when the hepatic stellate cell line was stimulated by angiotension II in our previous study. But the role of the GABA(B) receptor in liver fibrosis has never been reported. In the present study, we investigated the effects of this receptor on carbon tetrachloride-induced liver fibrosis in rats. The rats were divided into four groups including GABA(B) receptor agonist, antangonist, model and control group. alpha-smooth muscle actin (alpha-SMA) and GABA(B) receptor expression levels were detected by immunohistochemistry and real-time polymerase chain reaction. Liver function tests were performed once blood samples was taken; Western blot analysis was used to detect protein expression level of alpha-SMA and TGF-beta 1. We found baclofen ameliorated the CCl4-induced rats's liver fibrosis. The highest liver enzymes and alpha-SMA protein levels were found in the CGP35348 group. The GABA(B) receptor may have a protective role in the liver.
引用
收藏
页码:1909 / 1915
页数:7
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