γ-氨基丁酸 B 受体可改善大鼠四氯化碳诱导的肝纤维化。
Γ-aminobutyric acid B receptor improves carbon tetrachloride-induced liver fibrosis in rats.
机构信息
Institute of Organ Transplantation, 309th Hospital of Chinese People's Liberation Army, A17, Heishanhu Road, Haidian District, 100091 Beijing, China.
出版信息
Dig Dis Sci. 2013 Jul;58(7):1909-15. doi: 10.1007/s10620-013-2623-z. Epub 2013 Mar 19.
BACKGROUND
It was well known that angiotension II can inhibit hepatic stellate cell activation. The GABAB receptor was upregulated when the hepatic stellate cell line was stimulated by angiotension II in our previous study. But the role of the GABAB receptor in liver fibrosis has never been reported.
AIM
In the present study, we investigated the effects of this receptor on carbon tetrachloride-induced liver fibrosis in rats.
METHODS
The rats were divided into four groups including GABAB receptor agonist, antangonist, model and control group. α-smooth muscle actin (α-SMA) and GABAB 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 α-SMA and TGF-β1.
RESULTS
We found baclofen ameliorated the CCl4-induced rats's liver fibrosis. The highest liver enzymes and α-SMA protein levels were found in the CGP35348 group.
CONCLUSION
The GABAB receptor may have a protective role in the liver.
背景
众所周知，血管紧张素 II 能抑制肝星状细胞的激活。在我们之前的研究中，当肝星状细胞系受到血管紧张素 II 刺激时，GABAB 受体上调。但 GABAB 受体在肝纤维化中的作用尚未见报道。
目的
本研究旨在探讨该受体在大鼠四氯化碳诱导肝纤维化中的作用。
方法
将大鼠分为 GABAB 受体激动剂组、拮抗剂组、模型组和对照组 4 组。采用免疫组织化学和实时聚合酶链反应检测α-平滑肌肌动蛋白（α-SMA）和 GABAB 受体的表达水平。采集血样后进行肝功能检查；采用 Western blot 分析检测α-SMA 和 TGF-β1 的蛋白表达水平。
结果
我们发现巴氯芬改善了 CCl4 诱导的大鼠肝纤维化。CGP35348 组的肝酶和α-SMA 蛋白水平最高。
结论
GABAB 受体可能在肝脏中具有保护作用。
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