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

Background It was well known that angiotension II can inhibit hepatic stellate cell activation. The GABA.sub.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.sub.B 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 GABA.sub.B receptor agonist, antangonist, model and control group. [alpha]-smooth muscle actin ([alpha]-SMA) and GABA.sub.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. Results We found baclofen ameliorated the CCl.sub.4-induced rats's liver fibrosis. The highest liver enzymes and [alpha]-SMA protein levels were found in the CGP35348 group. Conclusion The GABA.sub.B receptor may have a protective role in the liver.