Antler thymosin β10 reduces liver fibrosis via inhibiting TGF-β1/SMAD pathway

Abstract

Hepatic stellate cell (HSC) activation is a crucial step in the development of liver fibrosis. Previous studies have shown that antler stem cells (AnSCs) inhibited HSC activation, suggesting that this may be achieved through secreting or releasing peptides. This study aimed to investigate whether AnSC-derived peptides (AnSC-P) could reduce liver fibrosis. The results showed that AnSC-P effectively reduced liver fibrosis in rats. Furthermore, we found that thymosin β10 (Tβ-10) was rich in AnSC-P, which may be the main component of AnSC-P contributing to the reduction in liver fibrosis. A further study showed that Tβ-10 reduced liver fibrosis in rats, with a reduction in HYP and MDA levels in the liver tissues, a decrease in the serum levels of ALP, ALT, AST, and TBIL and an increase in TP and ALB. Moreover, Tβ-10 decreased the expression levels of the genes related to the TGF-β/SMAD signaling pathway in vivo. In addition, Tβ-10 also inhibited TGF-β1-induced HSC activation and decreased the expression levels of the TGF-β/SMAD signaling pathway-related genes in HSCs in vitro. In conclusion, antler Tβ-10 is a potential drug candidate for the treatment of liver fibrosis, the effect of which may be achieved via inhibition of the TGFβ/SMAD signaling pathway.

Keywords: HSC activation; Liver fibrosis; Thymosin β10.