Thymosin-β4 inhibits proliferation and induces apoptosis of hepatic stellate cells through PI3K/AKT pathway

Liver fibrosis is a necessary stage for chronic liver diseases, and serious threat to human health. Hepatic fibrosis is a necessary stage for chronic liver diseases. Hepatic stellate cells (HSCs) are the primary cell type responsible for fibrosis. Thymosin beta 4 (T beta 4) has a potential role in the pathogenesis of liver fibrosis and that it is especially associated with the activation of HSCs, however, the underlying mechanisms are not fully elucidated. Herein, we investigated the potential role of T beta 4 in liver fibrosis by describing the effects of T beta 4, and we discuss the possible signaling pathway regulated by T beta 4. The expression of T beta 4 was significantly decreased in human HSC cell line LX-2 and CCl4-treated mouse liver. The depletion of T beta 4 significantly associated with the activation of HSCs via the enhanced expression of alpha-SMA and vimentin. T beta 4 significantly suppressed the viability and migration of HSCs. Understanding the potential effects and regulatory mechanism of T beta 4 in liver fibrosis might help to provide a novel treatment for patients with liver fibrosis.