动物造模,自发性高血压大鼠 z-bio 2021-11-15 279

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

　　Method: Take 16 male SHR rats and randomly divide them into SHR intervention group (captopril 10 mg/kg?D) and SHR control group (distilled water), 8 in each group and 8 in normal control group. Give captopril 10 mg/kg to SHR rats? D and distilled water for a total of 8 weeks. The blood pressure in the tail artery of the rat was measured before and after the model, and the rat was sacrificed 8 weeks later due to hemorrhage of the femoral artery. HE staining to observe the morphological changes of the rat heart. Western blot detection using real-time fluorescent quantitative polymerase chain reaction (qRT-PCR) to detect (AngⅡ) miRNA-137, transforming growth factor beta1 (transforming growth factor beta1, TGF-β1), angiotensin II (AngII), Smad protein 3 Expression) is detected. The expression levels of Smallmotheragaststcapen-taplegic protein 3 (Smad3), type I collagen (Col-I) and type III collagen (Col-III).

　　Result: The expression levels of miRNA-137, AngII, TGF-β1, Smad3, Col-I and Col-III in the heart of SHR rats are higher than those of Wistar rats (P\u003c0.01 or P\u003c0.05). The SHR intervention group was larger, the rat cardiomyocytes were significantly smaller than the SHR control group, and the cells were tightly arranged. The expressions of miRNA-137, AngII, TGF-β1, Smad3, Col-I and Col-III were significantly reduced (P\u003c0.01 or P\u003c0.05).

　　Conclusion: miRNA-137 may promote SHR cardiac remodeling by up-regulating Ang II and TGF-β1/Smads signaling pathway; Captopril intervention may inhibit the expression of miRNA-137.