AIM:To investigate the expression of poly(ADP-ribose) polymerase-2 (PARP-2) during rat car-diac hypertrophy in vitro and in vivo, and to explore the effects of PARP-2 on the cardiac hypertrophy.METHODS:Ab-dominal aortic coarctation ( AAC) was performed to establish a model of pressure overload-induced cardiac hypertrophy in SD rats.The expression of PARP-2 at mRNA and protein levels in the myocardium was determined by real-time PCR and Western blot.The hypertrophy model of the cardiomyocytes was induced by treating the cells with angiotensinⅡ( AngⅡ) . PARP-2 was knocked down by siRNAs in neonatal rat cardiomyocytes and the cardiomyocyte hypertrophy was evaluated by measuring the mRNA levels of ANF, BNP, and β-MHC and the cellular surface area.RESULTS: The expression of PARP-2 at mRNA and protein levels was both increased in the AAC rats as compared with those in the sham animals.The expression of PARP-2 at mRNA and protein levels was also increased in a time-and concentration-dependent manner in AngⅡ-induced hypertrophy model of the cardiomyocytes.In the neonatal rat cardiomyocytes, knockdown of PARP-2 ex-pression by siRNA attenuated AngⅡ-induced cardiac hypertrophy of the cardiomyocytes, indicating that endogenous PARP-2 played a positive regulatory role in cardiac hypertrophy.CONCLUSION:The mRNA and protein levels of PARP-2 in-crease in the in vitro and in vivo models of cardiac hypertrophy.Knockdown of PARP-2 protects cardiomyocytes from hyper-trophy.%目的：在细胞和整体水平研究多聚腺苷酸二磷酸核糖基聚合酶2（PARP-2）在心肌肥大过程中表达的变化规律以及PARP-2对心肌肥大的调控作用。方法：健康雄性SD大鼠采用腹主动脉缩窄法（ AAC）建立心肌肥大动物模型，采用real-time PCR和Western blot检测PARP-2的mRNA和蛋白表达变化；使用PARP-2特异性的siRNA干扰序列来处理细胞后，通过检测心肌细胞表面积及ANF、BNP和β-MHC的mRNA表达变化来作为评判心肌细胞肥大状况。结果：AAC大鼠心脏组织中PARP-2的蛋白和mRNA表达均显著上调；在AngⅡ诱导的心肌细胞肥大模型中，AngⅡ能时间和剂量依赖性地上调PARP-2的 mRNA和蛋白表达；用siRNA干扰序列沉默PARP-2能够逆转AngⅡ所诱导心肌细胞的肥大。结论：在AngⅡ诱导的心肌细胞肥大的体外模型和腹主动脉缩窄诱导的心肌肥大动物的体内模型中，PARP-2的mRNA和蛋白水平均显著上调；特异性沉默PARP-2能够抑制AngⅡ诱导的心肌细胞肥大。
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