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目的利用体外培养的乳鼠心肌细胞,观察吡格列酮对高浓度葡萄糖与去甲肾上腺素共同诱导的肥大心肌细胞的影响,进一步推测吡格列酮对糖尿病性心肌肥大的可能作用及作用机制。方法以培养的乳鼠心肌细胞为模型分组给药后,用显微镜目镜计数心肌细胞搏动的频率;用Lowry’s法测心肌细胞的蛋白质含量;用[3H]leucine标记法测定心肌细胞蛋白的合成;利用计算机图象分析系统测心肌细胞的体积。结果吡格列酮在1～10μmol·L-1浓度对25.5mmol·L-1高糖与1μmol·L-1去甲肾上腺素联合诱导的肥大心肌细胞的蛋白含量、蛋白合成及体积均有显著的抑制作用。其抑制肥大的效果比1μmol·L-1维拉帕米更为显著;同时观察到10μmol·L-1吡格列酮同1μmol·L-1维拉帕米一样有抑制心肌细胞搏动的作用。结论吡格列酮能有效抑制高糖与去甲肾上腺素联合诱导的心肌细胞肥大。这种作用可能是通过作用于PPARγ来实现的。
OBJECTIVE: To investigate the effect of pioglitazone on hypertrophic cardiomyocytes co-induced by high glucose and norepinephrine in neonatal rat cardiomyocytes cultured in vitro and to further speculate on the possible effect and mechanism of pioglitazone on diabetic cardiomyocyte hypertrophy. Methods The cultured neonatal rat cardiomyocytes were used as the model group, and then the beating frequency of cardiomyocytes was measured by microscope eyepiece. The protein content of cardiomyocytes was measured by Lowry’s method. Cardiomyocyte protein synthesis was measured by [3H] leucine labeling method. Computerized image analysis system to measure the volume of cardiomyocytes. Results Pioglitazone significantly inhibited the protein content, protein synthesis and volume of hypertrophic cardiomyocytes induced by 25.5 mmol·L-1 high glucose and 1 μmol·L-1 norepinephrine at the concentration of 1 ~ 10 μmol·L-1 . The effect of inhibiting hypertrophy was more significant than that of 1μmol·L-1 verapamil. Meanwhile, pioglitazone at 10μmol·L-1 was shown to inhibit cardiomyocyte pulsatility similarly to 1μmol·L-1 verapamil. Conclusion Pioglitazone can effectively inhibit cardiomyocyte hypertrophy induced by high glucose and norepinephrine. This effect may be through the role of PPARγ to achieve.