γ-aminobutyric acid B receptor (GABABR)ameliorated liver fibrosis by inhibiting hepatic cell migration
10.3760/cma.j.issn.1007-8118.2012.08.015
- VernacularTitle:γ-氨基丁酸B受体抑制大鼠肝细胞迁移并改善肝纤维化
- Author:
Wenmei FAN
;
Bingyi SHI
;
Kai FENG
;
Xihui MA
;
Hongshan WEI
;
Haiyan HUANG
;
Xiuyun HE
- Publication Type:Journal Article
- Keywords:
Liver fibrosis;
γ-aminobutyric acid;
Cell migration
- From:Chinese Journal of Hepatobiliary Surgery
2012;18(8):627-630
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the role of r-aminobutyric acid B receptor in the development of liver fibrosis.Methods Thirty-two Sprague-Dawley (SD) rats were divided into four groups including a control group,a model group,a baclofen group,and a CGP35348 group.Liver fibrosis was then induced by carbon tetrachloride (CCl4).Baclofen and CGP35348 treatment were carried out after the formation of liver fibrosis,followed by complete extraction of the eyeball to obtain blood sample to test liver function.Liver tissue specimens were cut and stored for histological staining,histochemistry,real-time polymerase chain-reaction (RT-PCR),and western blot analysis.Results Histological staining indicated that the degree of liver fibrosis was more severe in the CGP35348 group than in the baclofen group (P＜0.001).The levels of alanine transaminase (ALT),aspartate aminotransferase (AST),gamma-glutamyl transferase (GGT),total bilirubin (TBil),and direct bilirubin (DBil) were significantly lower in the baclofen group than in the CGP35348 group (P＜0.01).The levels of ALT,AST,GGT,TBil,and DBil were significantly higher in the CGP35348 group than in the model group (P＜0.05).Immunofluorescence results show that the hepatic cell migration was inhibited in the baclofen group.Western blot results showed that the expression levels of α-SMA protein were significantly lowered in the baclofen group when compared to that of the CGP35348 group and model group (P＜0.01).Conclusion GABAB receptor might play a role in the liver protection by inhibition of migration of hepatic cells in liver fibrosis.Further studies into the mechanism behind this function are further needed and may be a potential source of future anti-fibrotic treatment.
