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γ-Aminobutyric Acid B Receptor Improves Carbon Tetrachloride-Induced Liver Fibrosis in Rats
Ist Teil von
Digestive diseases and sciences, 2013-07, Vol.58 (7), p.1909-1915
Ort / Verlag
Boston: Springer US
Erscheinungsjahr
2013
Quelle
MEDLINE
Beschreibungen/Notizen
Background
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.
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
B
receptor agonist, antangonist, model and control group. α-smooth muscle actin (α-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 α-SMA and TGF-β1.
Results
We found baclofen ameliorated the CCl
4
-induced rats’s liver fibrosis. The highest liver enzymes and α-SMA protein levels were found in the CGP35348 group.
Conclusion
The GABA
B
receptor may have a protective role in the liver.