欢迎访问《中国实验方剂学杂志》编辑部网站!
冠心Ⅴ号合剂对大鼠急性心肌梗死后心室重构的作用及机制
作者:
作者单位:

作者简介:

通讯作者:

中图分类号:

基金项目:

南京市卫生局医学科技发展重点项目(201108005);江苏省普通高校研究生科研创新计划项目(CXZZ13_0)


Effect and Mechanism of Guanxin Ⅴ Mixture on Ventriculan Remodeling after Acute Myocardial Infarction
Author:
Affiliation:

Fund Project:

  • 摘要
  • |
  • 图/表
  • |
  • 访问统计
  • |
  • 参考文献
  • |
  • 相似文献
  • |
  • 引证文献
  • |
  • 资源附件
  • |
  • 文章评论
    摘要:

    目的: 观察冠心Ⅴ号合剂对急性心肌梗死(AMI)后心室重构的作用,探讨冠心Ⅴ号合剂改善心室重构的机制。方法: 雄性SD大鼠56只,随机分为空白组、假手术组、模型组、冠心Ⅴ号合剂临床等剂量组,2,4倍剂量组(0.5,1,2 g·kg-1),血脂康组(12.5 g·kg-1)。采用冠状动脉左前降支结扎法建立急性心肌梗死模型,各组模型鼠造模成功24 h后开始灌胃给药1次/d,连续4周,以心脏彩超测量射血分数(EF),缩短分数(FS),计算体表面积及左室心肌质量指数(LVMI),用Western blot技术检测Toll样受体4(TLR4),髓样分化因子(MyD88),核因子-κB/P65(NF-κB/p65)蛋白表达。结果: 与空白组、假手术组比较,模型组大鼠EF,FS降低,LVMI升高,梗死区心肌组织TLR4,MyD88,NF-κB/p65蛋白表达上调,差异有统计学意义(P<0.05);与模型组比较,冠心Ⅴ号合剂干预组各组大鼠EF,FS升高,LVMI降低,梗死区心肌组织TLR4,MyD88,NF-κB/p65蛋白表达降低,差异有统计学意义(P<0.05)。结论: 冠心Ⅴ号合剂能够抑制TLR4/MyD88/NF-κBp65信号通路,改善心室结构及心功能,从而干预心肌梗死后心室重构。

    Abstract:

    Objective: To observe the effect of Guanxin V mixture on acute myocardial infarction (AMI) after the ventricular remodeling, and investigate the mechanism of Guanxin V improving ventricular remodeling. Method: The model of acute myocardial infarction was established by left anterior descending coronary artery ligation. All of the rats were treated with Guanxin V mixture and Xuezhikang capsule for 4 weeks,The heart color measurement of ejection fractions (EF) value, fractional shortening (FS) value, calculate the left ventricular mass index and left ventricular surface area were observed,Western blot technique was used to detect the expression of Toll like receptor 4 (TLR4), myeloid differentiation factor 88(MyD88), nuclear factor-kappa B/p65 (NF-κB/p65) proteins. Result: Compared with the normal group and sham operation group,the EF,FS and expression of TLR4,MyD88,NF-κB/p65 in model rats were up-regulated, left ventricular mass index(LVMI) was decreased,the difference was statistically significant(P<0.05),Compared with the model group,the EF,FS and expression of TLR4,MyD88,NF-κB/p65 in model rats were decreased,LVMI was increased,the difference was statistically significant(P<0.05).Expression of Guanxin V mixture was inversely proportional to the concentration of protein,the difference was statistically significant(P<0.05). Conclusion: Guanxin V mixture can inhibit TLR4/MyD88/NF-κB p65 signal pathway,this may be one of the mechanisms of improving ventricular remodeling.

    参考文献
    相似文献
    引证文献
引用本文

左可可,柯峰,顾宁.冠心Ⅴ号合剂对大鼠急性心肌梗死后心室重构的作用及机制[J].中国实验方剂学杂志,2015,21(5):147~150

复制
分享
文章指标
  • 点击次数:
  • 下载次数:
  • HTML阅读次数:
  • 引用次数:
历史
  • 收稿日期:2014-08-02
  • 最后修改日期:
  • 录用日期:
  • 在线发布日期: 2015-03-01
  • 出版日期:

地址:北京东直门内南小街16号

邮编:100700

电话:010-84076882

E-mail:syfjx_2010@188.com

中国实验方剂学杂志 ® 2024 版权所有

技术支持:北京勤云科技发展有限公司