首页> 美国卫生研究院文献>Molecular Medicine Reports >Tormentic acid inhibits H2O2-induced oxidative stress and inflammation in rat vascular smooth muscle cells via inhibition of the NF-κB signaling pathway
【2h】

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

机译:甲酸通过抑制NF-κB信号通路抑制H2O2诱导的氧化应激和大鼠血管平滑肌细胞炎症

代理获取
本网站仅为用户提供外文OA文献查询和代理获取服务,本网站没有原文。下单后我们将采用程序或人工为您竭诚获取高质量的原文,但由于OA文献来源多样且变更频繁,仍可能出现获取不到、文献不完整或与标题不符等情况,如果获取不到我们将提供退款服务。请知悉。

摘要

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.
机译:甲酸(TA)是从植物Vochysia divergens的茎皮中分离出的三萜,据报道具有抗癌,抗炎和抗动脉粥样硬化特性。但是,TA在过氧化氢(H2O2)诱导的氧化应激和大鼠血管平滑肌细胞(RVSMCs)炎症中的功能尚不清楚。因此,本研究旨在研究TA是否抑制RVSMC中H2O2诱导的氧化应激和炎症,并确定其分子机制。本研究表明TA抑制了RVSMCs中活性氧(ROS)的产生,诱导了H2O2的表达,并抑制了H2O2诱导RVSMCs中的诱导型一氧化氮合酶(iNOS)和NADPH氧化酶(NOX)的表达。此外,TA显着降低了肿瘤坏死因子-α(TNF-α),白介素6(IL-6)和IL-1β的产生。此外,TA预处理可防止HSMC中H2O2诱导的核因子-κB(NF-κB)亚基p65磷酸化和NF-κB抑制剂α(IκBα)降解。因此,建议通过抑制NF-κB信号通路来抑制HSMC中H2O2诱导的氧化应激和炎症。 TA可能具有预防或治疗动脉粥样硬化的药理作用。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
代理获取

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号