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

作者：Luo, Huanhuan; Li, Liang; Tang, Jianbang; Zhang, Fengxue; Zhao, Fang; Sun, Da; Zheng, Fengling; Wang, Xinhua^*

来源：Molecular & Cellular Toxicology, 2016, 12(3): 265-271.

DOI：10.1007/s13273-016-0031-0

• Amygdalin
• HSC-T6 cells
• Fibrosis
• TGF-beta/CTGF

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 anti fibrotic 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-beta (TGF-beta) were decreased in HSC-T6 cells during amygdalin treatment. Secondly, to investigate functional role of TGF-beta, both TGF-beta over-expression vector and siRNA against TGF-beta were transfected into HSC-T6 cells respectively. The results showed that over-expression of TGF-beta promoted proliferation of HSC-T6 cells, whereas TGF-beta knockdown inhibited cell viability. Moreover, our data even indicated that TGF-beta could promote cell proliferation independent of amygdalin treatment. Finally, we found amygdalin could inhibit expression of the classical fibrotic factor alpha SMA, which suggested an antifibrotic effect of amygdalin. While the TGF-beta 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 HSC-T6 cell treated by amygdalin, but was up-regulated when exogenous TGF-beta introduced. As CTGF was one of the downstream factors in the TGF-beta pathway. These might suggest that amygdalin inhibited HSC-T6 cells proliferation and fibrosis via TGF-beta/CTGF pathway.

• 出版日期2016-9-30
• 单位广州中医药大学; 广州医科大学; 深圳华大生命科学研究院