| Objective: To investigation the effects of Magnesium isoglycyrrhizinate TGF-β/Smad signal expression in cultured HSC stimulated by TGF-β1 and then to reveal the possible molecular mechanism of Magnesium isoglycyrrhizinate on anti-fibrosis.Methods: The mice HSC-T6 were isolated and cultured with or without Magnesium isoglycyrrhizinate(0,0.01,0.1,1,10mg/ml)in vitro after TGF-β1 stimulation。The inhibitory rate of proliferation was measured by MTT method, the viability of cells was tested by evaluation of supernant LDH exclusion. The mRNA level of TGF-β1,Smad3, Smad 7 were measured with RT-PCR.Results:MTT method showed an obvious inhibition of HSC proliferation after Magnesium isoglycyrrhizinate(0,0.01,0.1,1,10mg/ml)treatment. Different concentrations of Magnesium isoglycyrrhizinate do not affect the vitality on HSC by LDH measurement。Different concentrations of Magnesium isoglycyrrhizinate increased the mRNA level of TGF-β1, Smad 3,Smad7 in HSC-T6; the expression of TGF-β1 and Smad3,Smad7 as the same as the expression of the trend. Different concentrations of magnesium isoglycyrrhizinate showed a certain trend of dose-effect relationship, with statistical difference.Conclusion: Magnesium isoglycyrrhizinate has significant impact on rat hepatic fibrosis liver TGF-β/ Smad signaling expression Inhibited rat hepatic stellate cell growth and proliferation, and its mechanism may be reduce the expression of TGF-β1, Smad3,Smad7 mRNA .
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