Huangqi Decoction reduces liver fibrosis in rats by modulating PI3K/Akt/mTOR signaling and promoting autophagy.

Liver fibrosis is a chronic condition caused by various factors, and currently, there are no widely effective treatments. Autophagy plays a crucial role in maintaining liver energy homeostasis, and its disruption can contribute to the development of liver fibrosis. This study investigates the effects and molecular mechanisms of Huangqi Decoction, a traditional Chinese medicine, on autophagy and apoptosis in fibrotic liver tissue. Tissue staining indicated that Huangqi Decoction mitigated CCL4-induced liver injury and apoptosis in rats. Western blot analysis of liver fibrosis markers revealed that Huangqi Decoction significantly reduced the expression levels of alpha-smooth muscle actin (α-SMA), type I collagen, matrix metalloproteinase-2 (MMP-2), and matrix metalloproteinase-9 (MMP-9). Additionally, serum markers of liver fibrosis and biochemical indicators of hepatocyte injury showed that Huangqi Decoction effectively lowered serum levels of hyaluronic acid (HA), lymph node (LN), type I collagen, aspartate aminotransferase (AST), and alanine aminotransferase (ALT). Furthermore, Western blot analysis confirmed that Huangqi Decoction alleviated hepatocyte injury by promoting autophagy and inhibiting the PI3K/Akt/mTOR signaling pathway. In conclusion, Huangqi Decoction enhances autophagy and inhibits apoptosis through the PI3K/Akt/mTOR pathway in rats with liver fibrosis.