MicroRNA-137与AngⅡ在自发性高血压大鼠心脏重构中的作用
作者:

Effects of MicroRNA-137 and Ang Ⅱ on cardiac remodeling in spontaneously hypertensive rats
Author:
  • 摘要
  • | |
  • 访问统计
  • |
  • 参考文献
  • |
  • 相似文献
  • |
  • 引证文献
  • | |
  • 文章评论
    摘要:

    目的 探讨微小核糖核酸195(MicroRNA-137,miRNA-137)、TGF-β1/Smads信号转导通路及血管紧张素Ⅱ(AngⅡ)在自发性高血压大鼠(SHR)心脏重构中的作用。方法 取雄性SHR大鼠16只,随机分为SHR干预组(卡托普利10 mg/kg·d)和SHR对照组(蒸馏水)各8只,另取Wistar大鼠8只为正常对照组,分别给予SHR大鼠卡托普利10 mg/kg·d和蒸馏水灌服,共持续8周。造模前后测大鼠尾动脉血压,8周后股动脉放血处死大鼠,HE染色观察大鼠心脏形态学改变,实时荧光定量多聚酶链式反应(qRT-PCR)法检测大鼠心脏中miRNA-137的表达,Western-blot检测转化生长因子β1(transforming growth factor beta1,TGF-β1)、血管紧张素Ⅱ(AngⅡ)、Smad蛋白3(small mother against decapen-taplegic protein three,Smad3)、I型胶原(Col-Ⅰ)和Ⅲ型胶原(Col-Ⅲ)蛋白表达水平。结果 SHR大鼠心脏miRNA-137、AngⅡ、TGF-β1、Smad3、Col-Ⅰ及Col-Ⅲ的表达量均高于Wistar大鼠(P<0.01或P<0.05),SHR干预组大鼠心肌细胞较SHR对照组明显变小,细胞排列较其紧密有序,miRNA-137、AngⅡ、TGF-β1、Smad3、Col-Ⅰ及Col-Ⅲ表达量均明显降低(P<0.01或P<0.05)。结论 miRNA-137可能通过上调AngⅡ及TGF-β1/Smads信号转导通路促进SHR心脏重构;卡托普利干预可抑制miRNA-137表达。

    Abstract:

    Objective To investigate the role of small RNA 195 (MicroRNA-137), TGF-β1/Smads signal transduction pathway and angiotensin Ⅱ (Ang Ⅱ) in cardiac remodeling in spontaneously hypertensive rats (SHR). Methods 16 SHR male rats were randomly divided into intervention group SHR (captopril 10 mg/kg·d) and SHR control group (distilled water), the other 8 Wistar rats were normal control group, rats were given captopril 10 mg/kg·d or distilled water for 8 weeks. Caudal arterial pressure was measured before and after the intervention, intervention after 8 weeks rats were killed by exsanguination, HE staining was used to observe the morphological changes of rat heart, qRT-PCR method was used to detect the expression of miRNA-137 in rat heart, Western-blot detection of TGF-β1 and Ang Ⅱ, Smad 3, Col-Ⅰand Col-Ⅲ protein. Results Compared to the normal control groups,the miRNA-137,AngⅡ,TGF-β1,Smad3,Col-Ⅰand Col-Ⅲ were higher expressed in SHR treatment group and SHR control groups(P<0.01 or P<0.05); Compared to the SHR control group,the cardiomyocyte of SB group becomes smaller and arranged more closely and orderly,the miRNA-137,AngⅡ,TGF-β1,Smad3,Col-Ⅰand Col-Ⅲ were significantly lower expressed(P<0.01 or P<0.05). Conclusions MiRNA-137 may promote SHR cardiac remodeling by up regulation of Ang Ⅱ and TGF-β1/Smads signaling pathway; the captopril intervention can inhibit miRNA-137 expression.

    参考文献
    相似文献
    引证文献
引用本文

侯永兰,李石林,刘玲玲. MicroRNA-137与AngⅡ在自发性高血压大鼠心脏重构中的作用[J].中国比较医学杂志,2016,26(7):52~56.

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
  • 最后修改日期:2016-01-11
  • 在线发布日期: 2016-07-28
防诈骗提示!请勿点击不明链接或添加个人微信。编辑部所有邮箱后缀均为@cnilas.org
关闭