...
首页> 外文期刊>Tropical Journal of Pharmaceutical Research >Schisandra chinensis extract ameliorates myocardial ischemia/reperfusion injury via TLR4/NF-κB/MyD88 signaling pathway
【24h】

Schisandra chinensis extract ameliorates myocardial ischemia/reperfusion injury via TLR4/NF-κB/MyD88 signaling pathway

机译:Schisandra Chinensis提取物改善了通过TLR4 / NF-κB/ MYD88信号通路的心肌缺血/再灌注损伤

获取原文
           

摘要

Purpose: To investigate the effects of Schisandra chinensis extract (SCE) on myocardial ischemia-reperfusion (I/R) injury and to elucidate its underlying mechanism of action. Methods: A rat model of myocardial I/R injury was used. Ischemia was induced by occluding the left anterior descending artery for 30 min and the myocardium was then reperfused for 2 h in Sprague-Dawley rats. Triphenyltetrazolium chloride (TTC) staining was used to measure myocardial infarct size, while the levels of inflammatory cytokines were evaluated by enzyme-linked immunosorbent assay (ELISA). Western blot assay was conducted to determine protein levels. Results: TTC staining showed that myocardial I/R injury was ameliorated after SCE treatment. Serum creatine kinase (CK), lactate dehydrogenase (LDH), and malondialdehyde (MDA) levels decreased, whereas superoxide dismutase (SOD) activity increased after SCE treatment. Moreover, serum interleukin-1β (IL-1β), IL-6, and tumor necrosis factor-α (TNF-α) ex pression levels were reduced after SCE treatment. Furthermore, SCE treatment remarkably downregulated the protein ex pression levels of Toll-like receptor 4 (TLR4), nuclear factor-kappa B (NF-κB), and myeloid differentiation factor 88 (MyD88). Conclusion: SCE may exert protective effects against myocardial I/R injury by downregulating TLR4-mediated NF-κB/MyD88 signaling pathway. However, this needs to confirmed in clinical studies.
机译:目的:探讨Schisandra Chinensis提取物(SCE)对心肌缺血再灌注(I / R)伤害的影响,并阐明其基本行动机制。方法:使用了心肌I / R损伤的大鼠模型。通过封闭左前动脉30分钟的缺血诱导,然后在Sprague-Dawley大鼠中再灌注心肌。使用酶联免疫吸附测定(ELISA)评估三苯基四唑氯化物(TTC)染色来测量心肌梗塞尺寸,而炎症细胞因子的水平评估。进行蛋白质印迹测定以确定蛋白质水平。结果:TTC染色表明,在SCE治疗后,心肌I / R损伤发生了改善。血清肌酸激酶(CK),乳酸脱氢酶(LDH)和丙二醛(MDA)水平降低,而SCE治疗后超氧化物歧化酶(SOD)活性增加。此外,在SCE治疗后,减少了血清白细胞介素-1β(IL-1β),IL-6和肿瘤坏死因子-α(TNF-α)EX Exclion水平。此外,SCE治疗显着下调了蛋白质Exclous级受体4(TLR4),核因子-Kappa(NF-κB)和骨髓分化因子88(MYD88)的蛋白质Exclation的压力水平。结论:通过下调TLR4介导的NF-κB/ MYD88信号通路,SCE可能对心肌I / R损伤产生保护作用。然而,这需要在临床研究中确认。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

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