Inhibitory effect of dietary capsaicin on liver fibrosis in mice

Scope Virtually all chronic liver injuries result in the activation of hepatic stellate cells (HSCs). In their activated state, these cells are the main collagen-producing cells implicated in liver fibrosis. Capsaicin (CPS), the active compound of chili peppers, can modulate the activation and migration of HSCs in vitro. Here, we evaluated the potential protective and prophylactic effects of CPS related to cholestatic and hepatotoxic-induced liver fibrosis and its possible underlying mechanism of action. Methods and results Male Balb/c mice received dietary CPS after 3 days of bile duct ligation (BDL) or before and during carbon tetrachloride (CCl4) injections. Mice receiving dietary CPS after BDL had a significant improvement of liver fibrosis accompanied by a decrease in collagen deposition and downregulation of activation markers in isolated HSCs. In the CCl4 model, dietary CPS inhibited the upregulation of profibrogenic markers. However, CPS could not attenuate the CCl4-induced fibrosis when it was already established. Furthermore, in vitro CPS treatment inhibited the autophagic process during HSC activation. Conclusion Dietary CPS has potential benefits in the therapy of cholestatic liver fibrosis and in the prophylaxis of hepatotoxic-induced liver injury.