中文摘要：

目的：研究Pim-2基因在过氧化氢（H2O2）诱导乳鼠心肌细胞损伤中的作用及三七皂苷R1的干预效应。方法：H2O2干预原代培养的乳鼠心肌细胞造成细胞损伤模型,分别以三七皂苷R1和Pim-2 RNAi干预细胞,MTT法检测细胞增殖,流式细胞术测细胞凋亡,实时定量PCR法测细胞内Pim-2 mRNA水平,Western blotting法测Pim-2、Bax及Bcl-2蛋白表达。结果：H2O2上调Pim-2 mRNA及蛋白水平,抑制细胞增殖与促进凋亡,与对照组相比差异有统计学意义（P〈0.001）。Pim-2基因沉默后,细胞活性降低,凋亡增加,LDH与MDA浓度增加,SOD活性降低,Bax蛋白表达增加,Bcl-2蛋白水平降低,与对照组相比差异有统计学意义（P〈0.001）。三七皂苷R1预处理能显著增加细胞活力,抑制细胞凋亡,上调Pim-2蛋白水平,与H2O2组相比差异有统计学意义（P〈0.001）。结论：Pim-2能减轻H2O2致心肌细胞损伤,可能与抗凋亡,抗氧化,调控凋亡相关蛋白Bax及Bcl-2表达有关;三七皂苷R1抗心肌细胞损伤与Pim-2有关。

英文摘要：

Objective： To study the effect of Pim-2 in cardiomyocytes damage induced by H2O2 and the prevention of Notoginsenoside R1. Methods： The primary cultured cardiomyocytes were stimulated by H2O2 to establish cellular injury model. Both Notoginsenoside R1 and Pim-2 RNAi were assayed. MTT assay was used to check cell proliferation and flow cytometry for cell apoptosis checking. Pim-2 mRNA was determined by real time PCR and protein level by western blotting. Results： H2O2 could induce cardiomyocytes damage and up-regulate both the levels of Pim-2 mRNA and protein. Pim-2 could anti-apoptosis and alleviate cardiomyocytes injury induced by H2O2. Notoginsenoside R1 could protect cardiomyocytes from damage by H2O2. Meanwhile,Notoginsenoside R1 could increase the level of Pim-2 protein and compared with that of H2O2 group,the difference was significant（ P〈0. 001）. Conclusion： Pim-2 can alleviate cardiomyocytes injury induced by H2O2,which is mainly related to anti-apoptosis and anti-oxidative stress,regulation of the expressions of Bax and Bcl-2. Notoginsenoside R1 protects cardiomyocytes from injury by H2O2 partly through the regulation of Pim-2.