Mangiferin alleviates lipopolysaccharide and D-galactosamine-induced acute liver injury by activating the Nrf2 pathway and inhibiting NLRP3 inflammasome activation

摘要

Mangiferin, a glucosylxanthone from Mangifera indica, has been reported to have anti-inflammatory effects. However, the protective effects and mechanisms of mangiferin on liver injury remain unclear. This study aimed to determine the protective effects and mechanisms of mangiferin on lipopolysaccharide (LPS) and D-galactosamine (D-GaIN)-induced acute liver injury. Mangiferin was given 1 h after LPS and D-GaIN treatment. The results showed that mangiferin inhibited the levels of serum ALT, AST, IL-1 beta, TNF-alpha, MCP-1, and RANTES, as well as hepatic malondialdehyde (MDA) and ROS levels. Moreover, mangiferin significantly inhibited IL-1 beta and TNIF-alpha production in LPS-stimulated primary hepatocytes. Mangiferin was found to up-regulate the expression of Nrf2 and HO-1 in a dose-dependent manner. Furthermore, mangiferin inhibited LPS/D-GaIN-induced hepatic NLRP3, ASC, caspase-1, IL-1 beta and TNIF-alpha expression. In conclusion, mangiferin protected against LPS/GaIN-induced liver injury by activating the Nrf2 pathway and inhibiting NLRP3 inflammasome activation. (C) 2015 Elsevier BY. All rights reserved.