MicroRNA-137与AngⅡ在自发性高血压大鼠心脏重构中的作用  

Effects of MicroRNA-137 and AngⅡ on cardiac remodeling in spontaneously hypertensive rats

作　　者：侯永兰[1] 李石林[1] 刘玲玲[1] 

机构地区：[1]河南省新乡市中心医院心内一科,河南新乡453000

出　　处：《中国比较医学杂志》2016年第7期52-56,共5页Chinese Journal of Comparative Medicine

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。Objective To investigate the role of small RNA 195 （MicroRNA-137）, TGF-131/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- I and Col-llI protein. Results Compared to the normal control groups, the miRNA-137, Ang I1 ,TGF-131, Smad3, Col- I and Col-Ⅲ were higher expressed in SHR treatment group and SHR control groups （P 〈 0. O1 or P 〈 O. 05 ） ; Compared to the SHR control group,the eardiomyocyte of SB group becomes smaller and arranged more closely and orderly, the miRNA-137, Ang II , TGF-131, Smad3, Col- I and Col-Ill were significantly lower expressed （ P 〈 0. O1 or P 〈 0.05 ）. Conclusions MiRNA-137 may promote SHR cardiac remodeling by up regulation of Ang II and TGF-~31/Smads signaling pathway; the eaptopril intervention can inhibit miRNA-137 expression.

关 键 词：心脏重构 miRNA-137 自发性高血压大鼠 TGF-β1/Smads信号通路 

分 类 号：R544.1[医药卫生—心血管疾病]