Background/Aims Angiotensin II (Ang II) plays an important role in the activation of hepatic stellate cells (HSCs). In this study it was found that expression of the GABAB receptor was elevated in HSCs treated with Ang II. We attempted to elucidate the mechanism of the GABAB receptor in HSCs activation. Methods First, the target gene (GABAB receptor) was screened by gene chip in HSCs treated with Ang II. Second, the biological function of the GABAB receptor was analyzed by MTT, cell-cycle assay, real-time PCR, and western blot. The methods of MTT and cell-cycle assay were used to evaluate the effect of the GABAB receptor on proliferation and DNA synthesis of HSCs. Expression of ECM, TGF-β1, and α-SMA was analyzed by real-time PCR and western blot. Results The GABAB receptor’s specific agonist CGP35348 inhibited the activation of HSCs, which could be partially reversed by the GABAB receptor’s antagonist. Conclusions Our in-vitro results demonstrated that the GABAB receptor could inhibit HSCs activation.
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