动物造模,自发性高血压 z-bio 2022-07-07 655

　　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 cardiac remodeling in spontaneously hypertensive rats (SHR). .

　　Methods: 16 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 were selected as normal control group , SHR rats were given captopril 10 mg/kg·d and distilled water, respectively, for 8 weeks. The blood pressure of the tail artery of the rats was measured before and after modeling, and the rats were sacrificed by bleeding from the femoral artery after 8 weeks. HE staining was used to observe the morphological changes of the rat heart, and real-time quantitative polymerase chain reaction (qRT-PCR) method was used to detect the miRNA- The expression of 137 was detected by Western-blot, 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). Compared with the SHR control group, the cells were significantly smaller, and the cell arrangement was more compact and orderly. The expressions of miRNA-137, AngⅡ, TGF-β1, Smad3, Col-Ⅰ and Col-Ⅲ were significantly decreased (P<0.01 or P<0.05). .

　　Conclusion: miRNA-137 may promote SHR cardiac remodeling by up-regulating AngⅡ and TGF-β1/Smads signal transduction pathways; captopril can inhibit the expression of miRNA-137.