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        Amygdalin inhibits HSC-T6 cell proliferation and fibrosis through the regulation of TGF-β/CTGF

        Huanhuan Luo,Liang Li,Jianbang Tang,Fengxue Zhang,Fang Zhao,Da Sun,Fengling Zheng,Xinhua Wang,Xinhua Wang 대한독성 유전단백체 학회 2016 Molecular & cellular toxicology Vol.12 No.3

        Amygdalin is one of the nitrilosides that was widely used to treat cancer, inhibit liver fibrosis. In the present study, the aim was to determine the antifibrotic potential of amygdalin and examine its mechanisms of action in vitro. Firstly, we found amygdalin significantly inhibited HSC-T6 cells proliferation. Both mRNA and protein of transforming growth factor-β (TGF-β) were decreased in HSC-T6 cells during amygdalin treatment. Secondly, to investigate functional role of TGF-β, both TGF-β over-expression vector and siRNA against TGF-β were transfected into HSC-T6 cells respectively. The results showed that over-expression of TGF-β promoted proliferation of HSC-T6 cells, whereas TGF-β knockdown inhibited cell viability. Moreover, our data even indicated that TGF-β could promote cell proliferation independent of amygdalin treatment. Finally, we found amygdalin could inhibit expression of the classical fibrotic factor αSMA, which suggested an antifibrotic effect of amygdalin. While the TGF-β antagonized anti-fibrotic effect of amygdalin. To assess the mechanisms, we examined expression of CTGF in cultured HSC-T6 cells. Our results showed that CTGF was down-regulated in HSCT6 cell treated by amygdalin, but was up-regulated when exogenous TGF-β introduced. As CTGF was one of the downstream factors in the TGF-β pathway. These might suggest that amygdalin inhibited HSC-T6 cells proliferation and fibrosis via TGF-β/CTGF pathway.

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