节点文献

银杏内酯K减轻氧糖剥夺对心肌细胞的坏死性凋亡研究

Ginkgolide K protects H9C2 cells against oxygen-glucose deprivation-induced apoptosis

  • 推荐 CAJ下载
  • PDF下载
  • 不支持迅雷等下载工具,请取消加速工具后下载。

【作者】 王京高燕马乔娟

【Author】 WANG Jing;GAO Yan;MA Qiao-juan;Department of Cardiology,Affiliated Hospital of Yan’an University;Department of Cardiology,Tongchuan Mining Bureau Central Hospital;

【通讯作者】 马乔娟;

【机构】 延安大学附属医院心内科陕西省铜川市矿务局中心医院心血管内科

【摘要】 目的探讨银杏内酯K对心肌缺血的保护作用及其作用机制。方法将H9C2心肌细胞暴露于氧糖剥夺(OGD)条件下,体外模拟缺血缺氧模型。暴露于OGD 4 h后,给予不同浓度(12. 5μg/ml、25μg/ml、50μg/ml)的银杏内酯K孵育H9C2细胞1 h。对照组细胞仅在OGD实验时换为高糖DMEM,不做其他处理。培养结束后检测H9C2细胞的细胞活力、活性氧(ROS)含量;流式细胞术检测细胞凋亡;荧光实时定量PCR检测H9C2细胞内p38 MAPK和JNK的表达水平。结果与对照组相比,银杏内酯K能显著提高细胞活力,且呈剂量依赖性。与对照组相比,OGD组ROS含量显著增加(P <0. 05),不同浓度12. 5μg/ml、25μg/ml、50μg/ml的银杏内酯K处理H9C2细胞1 h,可显著减少各组细胞内ROS含量,抑制各组细胞凋亡,显著降低H9C2细胞内p38 MAPK和JNK的mRNA表达水平(P <0. 05),且呈剂量依赖性。结论银杏内酯K对体外模拟的心肌缺血具有保护作用,其作用机制与通过抑制ROS诱发的p38和JNK激活所致凋亡通路有关。

【Abstract】 Objective To investigate the protective effect and functional mechanism of Ginkgolide K on myocardial ischemia. Methods H9 C2 cells were exposed to oxygen-glucose deprivation( OGD) to simulate an ischemic model in vitro. After 4 hours of OGD exposure,H9 C2 cells were incubated with ginkgolide K at different concentrations( 12. 5 μg/ml,25 μg/ml,50 μg/ml) for 1 hour. The control cells were changed to high glucose DMEM only during the OGD experiment and no other treatment was performed. After the end of culture,the cell activity and ROS content of H9 C2 cells were detected,cell apoptosis was detected by flow cytometry,and the expression levels of p38 MAPK and JNK in H9 C2 cells were detected by real-time quantitative fluorescence PCR. Results Compared with the control group,Ginkgolide K significantly increased cell viability in a dose-dependent manner. Compared with the control group,the ROS content in the OGD group was significantly increased( P <0. 05). The treatment of H9 C2 cells treated with different concentrations of 12. 5 μg/ml,25 μg/ml and 50 μg/ml for 1 h could significantly reduce each group( P < 0. 05). The intracellular ROS content inhibited the apoptosis of each group and significantly decreased the expression of p38 MAPK and JNK mRNA in H9 C2 cells in a dose-dependent manner( P < 0. 05). Conclusion In conclusion,Ginkgolide K demonstrated a cardio-protective effect on myocardial ischemia in vitro,and this effect was mediated through the inhibition of the apoptosis pathway triggered by ROS-induced p38 and JNK activation.

【基金】 陕西省卫生厅项目(编号:SX13004023)
  • 【文献出处】 临床和实验医学杂志 ,Journal of Clinical and Experimental Medicine , 编辑部邮箱 ,2019年22期
  • 【分类号】R285.5
  • 【被引频次】1
  • 【下载频次】186
节点文献中: 

本文链接的文献网络图示:

本文的引文网络