Smad and mitogen-activated protein kinase (MAPK) protein expressions were detected using Western blot analysis. Cardiomyocyte hypertrophy indices, including cell surface area, protein content and incorporation were measured. The effects of blockade of endogenous BNP by its receptor antagonist, HS-142-1, on cell hypertrophy were investigated. Cardiomyocytes from neonatal rats were cultured and a cardiomyocyte hypertrophy model was established with angiotensin II (Ang II). In the present study, we examined the role of endogenous BNP on cardiomyocyte hypertrophy and the related molecular mechanisms. However, the mechanisms have not been fully elucidated. Our studies have shown that long-term treatment of rats with BNP attenuated cardiac hypertrophy via down-regulation of TGF-β1 and up-regulation of smad7. Previous studies suggest that B-type natriuretic peptide (BNP) exerts inhibitory effects on cardiac hypertrophy.
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