Tormentic acid inhibits H2O2-induced oxidative stress and inflammation in rat vascular smooth muscle cells via inhibition of the NF-κB signaling pathway

Wang,Yu‑Lun; Sun,Gen‑Yi; Zhang,Ying; He,Jia‑Jun; Zheng,Shen; Lin,Jing‑Na

doi:10.3892/mmr.2016.5690

Tormentic acid inhibits H2O2-induced oxidative stress and inflammation in rat vascular smooth muscle cells via inhibition of the NF-κB signaling pathway

Authors:
- Yu‑Lun Wang
- Gen‑Yi Sun
- Ying Zhang
- Jia‑Jun He
- Shen Zheng
- Jing‑Na Lin
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Affiliations: Department of Endocrinology, People's Hospital of Tianjin City, Tianjin 300121, P.R. China, Department of Cardiology, Tianjin Chest Hospital, Tianjin 300131, P.R. China, Department of Internal Medicine, Hongqiao Hospital of Tianjin City, Tianjin 300051, P.R. China
Published online on: August 30, 2016 https://doi.org/10.3892/mmr.2016.5690
Pages: 3559-3564
Copyright: © Wang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

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 (H2O2)‑induced oxidative stress and inflammation in rat vascular smooth muscle cells (RVSMCs) remain unclear. Therefore, the present study aimed to investigate whether TA suppressed H2O2‑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 H2O2 in RVSMCs, and inhibited H2O2-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 H2O2 in RVSMCs. TA is, therefore, suggested to inhibit H2O2-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.

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