| Objective: Rhizoma coptidis, the root of Coptis chinensis Franch, has been used as a folk medicine in the treatment of diabetes for thousands of years in China. Berberine, one of the active constituent of Rhizoma coptidis, has been reported to improve symptoms of diabetes and to treat experimental cardiac hypertrophy, respectively. This study investigated the potential effects of berberine on diabetic cardiomyocyte hypertrophy and its possible influence on peroxisome proliferator-activated receptor-α(PPARα)-nitric oxide (NO) signal pathway.Methods: The cultured neonatal rat cardiomyocyte was used to observe the effects of BBR on cardiomyocyte hypertrophy induced by HGI (glucose at 25.5 mmol/L and insulin at 0.1μmol/L ), and the cardiomyocyte hypertrophic responses were assayed by measuring the cell surface area, protein content, and atrial natriuretic factor (ANF) mRNA expression. The expressions of mRNA and protein were assayed by real time RT-PCR and Western blot. NO synthase (NOS) activity and NO concentration in media were determined with the spectrophotometry and Griess assay, respectively.Results: HGI significantly induced cardiomyocyte hypertrophy and decreased the expressions of PPARαand eNOS at both mRNA and protein levels (P<0.05), and also reduced NOS activity and NO concentration (P<0.01), which were increased by either berberine in a concentration-dependent manner (from 0.1 to 100μmol·L-1) or fenofibrate or L-Arginine (P<0.01). MK 886, a selective PPARαantagonist, could abolish the effects of berberine and fenofibrate (P<0.01). NG-nitro-L-Arginine-methyl ester, a NOS inhibitor, could block the effects of L-Arginine, but only partially blocked the effects of berberine (P<0.01).Conclusions: These results indicate that BBR can inhibit cardiomyocyte hypertrophy induced by HGI, which may be, at least partly, mediated by promoting the expression of PPARα, and then increasing the expression and activity of eNOS, elevating the release of NO. |
PDF Full Text Request