目的探讨罗格列酮(RSG)对成纤维细胞无血清条件培养液(FCGM)诱导心肌肥大的作用及其机制。方法分离获取新生大鼠成纤维细胞,用含10g/L胰岛素+转铁蛋白+硒化钠复合物(ITS)的无血清高糖DMEM培养,分别于第3、5、79、天收集FCGM,ELISA法检测其中内皮素-1(ET-1)的浓度。采用FCGM培养新生大鼠心肌细胞,检测其蛋白含量和蛋白激酶C(PKC)活性,并观察白屈菜季氨碱(che)、RSG对FCGM诱导心肌蛋白质合成的影响。结果 FCGM中含有ET-1,且培养3d时的浓度最高。FCGM可促进心肌细胞蛋白质合成,而RSG和che可阻断FCGM促心肌细胞蛋白质合成的作用并抑制心肌细胞PKC的活性。结论 FCGM诱导心肌肥大与其中的ET-1有关,RSG抑制心肌肥大的作用与抑制ET-1和PKC的活性有关。
Objective To investigate the inhibitory effect of rosiglitazone(RSG) on fibroblast conditioned growth medium(FCGM)-induced myocardial hypertrophy and its mechanism in rats.Methods FCGM-stimulated protein synthesis and protein kinase C(PKC) activity were measured in neonatal rat ventricular cardiomyocytes in the absence or presence of RSG or the PKC inhibitor chelerythrine(che).Results Cultured neonatal rat ventricular fibroblast conditioned growth medium significantly enhanced protein synthesis of cardiomyocytes.Meanwhile ET-1 was detected in FCGM using the enzyme-linked immunosorbent assay(ELISA).RSG and che counteracted the growth promoting effect of FCGM possibly via suppressing PKC activity.Conclusion FCGM-induced myocardial hypertrophy may be associated with ET-1.The inhibitory effects of RSG on myocardial hypertrophy may be mediated through ET-1 and PKC.