Salvianolic Acid B Inhibits High‐Fat Diet‐Induced Inflammation by Activating the Nrf2 Pathway

Abstract

Salvianolic acid B (Sal B) is a major water-soluble bioactive component of Salvia miltiorrhiza, which is a traditional Chinese medicine. We investigated the ways in which Sal B affects high-fat diet (HFD)-induced immunological function disorder remission using a C57BL/6 mouse model. We gave groups of C57BL/6 mice a normal diet (Control), a normal diet supplemented with Sal B (Control + Sal B), a high-fat diet (HF), and a high-fat diet supplemented with Sal B (HF + Sal B) for 10 wk. Sal B supplementation decreased the body weight and plasma lipids, increased the fecal excretion of lipids, prevented the accumulation of chronic oxidative stress, and reversed the disproportionality of CD3⁺ CD4⁺ and CD3⁺ CD8⁺ T lymphocytes compared to HFD. We found an increase in IL-6 and TNF-α, while IL-10 decreased in plasma after the HFD and Sal B reversed the deregulation of the Thl/Th2 ratio. In addition, HFD-induced inflammation was stopped by Sal B through the downregulation of nuclear factor-κB (NF-κB), cyclooxygenase-2 (COX-2), and inducible NO synthesis (iNOS), and the upregulation of nuclear factor-erythroid 2-related factor 2 (Nrf2)-regulated genes. These findings demonstrated that Sal B could effectively attenuate inflammation by activating the Nrf2-mediated antioxidant defense system.