摘要
目的探讨阿托伐他汀(atorvastatin,Ato)在异丙肾上腺素诱发的原代乳鼠心肌细胞肥大中所发挥的作用及机制。方法采用异丙肾上腺素(isoproterenol,ISO)10μmol/L建立原代乳鼠心肌细胞肥大模型。应用RT-PCR技术测定心肌肥厚指标心钠肽(ANP)、脑钠肽(BNP)的mRNA表达水平;采用激光扫描共聚焦技术测量细胞静息游离钙的含量;应用Western blot技术测定心肌肥厚信号转导通路Cn、NFAT的蛋白表达。结果与模型组相比,阿托伐他汀浓度为5、10μmol/L时ANP、BNP基因表达明显下调;ISO诱发的心肌细胞内钙的升高显著降低;Cn和NFAT的蛋白表达水平显著下调。结论阿托伐他汀能够抑制异丙肾上腺素诱发的原代乳鼠心肌细胞肥大,其作用机制可能与抑制钙离子介导的CnNFAT信号通路有关。
Objective To investigate the effects of atorvastatin （Ato） on isoproterenol （ISO）- induced cardiomyocyte hypertrophy and its mechanism. Methods Hypertrophy in neonatal rat ventricular myoeytes was induced by ISO. The mRNA level of the hypertrophic marker of ANP and BNP was detected by RT-PCR. The intracellular resting free calcium was detected by using laser scanning confocal microscope. The expression of calcineurin （Cn） and nuclear factor of activated T cells （NAFT） were detected by Western blot. Results The mRNA level of ANP and BNP, the increment of the resting intracellular free calcium induced by ISO and the ex- pression of Cn and NFAT were decreased by Ato （5,10μmol/L）. Conclusion The anti-hy- pertrophic effects of Ato on ISO-induced eardiomyocyte hypertrophy is associated with inhibition of calcium mediated Cn-NFAT signaling pathway.
出处
《哈尔滨医科大学学报》
CAS
2015年第4期305-308,共4页
Journal of Harbin Medical University
基金
黑龙江省教育厅科学技术研究项目(12531390)
