Tormentic acid inhibits H(2)O(2)-induced oxidative stress and inflammation in rat vascular smooth muscle cells via inhibition of the NF-κB signaling pathway

Tormentic acid (TA) is a triterpene isolated from the stem bark of the plant Vochysia divergens and has been reported to exhibit anticancer, anti-inflammatory and anti-atherogenic properties. However, the functions of TA in hydrogen peroxide (H(2)O(2))-induced oxidative stress and inflammation in rat vascular smooth muscle cells (RVSMCs) remain unclear. Therefore, the present study aimed to investigate whether TA suppressed H(2)O(2)-induced oxidative stress and inflammation in RVSMCs, and to determine its molecular mechanisms. The present study demonstrated that TA inhibited reactive oxygen species (ROS) generation, induced H(2)O(2) in RVSMCs, and inhibited H(2)O(2)-induced expression of inducible nitric oxide synthase (iNOS) and NADPH oxidase (NOX) in RVSMCs. In addition, TA significantly decreased the production of tumor necrosis factor-α (TNF-α), interleukin 6 (IL-6) and IL-1β. Furthermore, TA pretreatment prevented nuclear factor-κB (NF-κB) subunit p65 phosphorylation and NF-κB inhibitor α (IκBα) degradation induced by H(2)O(2) in RVSMCs. TA is, therefore, suggested to inhibit H(2)O(2)-induced oxidative stress and inflammation in RVSMCs via inhibition of the NF-κB signaling pathway. TA may have potential as a pharmacological agent in the prevention or treatment of atherosclerosis.