MicroRNA-137,自发性高血压 z-bo 2020-11-12 310

　　Objective: To investigate the role of microribonucleic acid 195 (MicroRNA-137, miRNA-137), TGF-β1/Smads signal transduction pathway and angiotensin Ⅱ (Ang Ⅱ) in spontaneously hypertensive rats (SHR) cardiac remodeling .

　　Methods: Sixteen male SHR rats were randomly divided into SHR intervention group (captopril 10 mg/kg·d) and SHR control group (distilled water), 8 rats each, and 8 Wistar rats as normal control group , SHR rats were given captopril 10 mg/kg·d and distilled water for a total of 8 weeks. The blood pressure of the rat’s tail artery was measured before and after the model. 8 weeks later, the rats were sacrificed by bleeding from the femoral artery. The morphological changes of the rat heart were observed by HE staining. The real-time fluorescent quantitative polymerase chain reaction (qRT-PCR) method was used to detect miRNA- 137 expression, Western-blot detection of transforming growth factor β1 (transforming growth factor beta1, TGF-β1), angiotensin II (Ang II), Smad protein 3 (small mother against decapen-taplegic protein three, Smad3), type I collagen (Col-Ⅰ) and type III collagen (Col-Ⅲ) protein expression levels.

　　Results: The expression levels of miRNA-137, AngⅡ, TGF-β1, Smad3, Col-Ⅰ, and Col-Ⅲ in the heart of SHR rats were higher than those of Wistar rats (P<0.01 or P<0.05). The myocardium of SHR intervention group The cells were significantly smaller than the SHR control group, and the cells were arranged tightly and orderly. The expression of miRNA-137, AngⅡ, TGF-β1, Smad3, Col-Ⅰ and Col-Ⅲ were all significantly reduced (P<0.01 or P<0.05) .

　　Conclusion: miRNA-137 may promote SHR cardiac remodeling through up-regulation of AngⅡ and TGF-β1/Smads signal transduction pathway; Captopril intervention can inhibit miRNA-137 expression.