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[目的]研究microRNA-21(miR-21)及其靶蛋白PDCD4在人参皂甙Rb1(GS-Rb1)保护缺血缺氧损伤心肌细胞中的作用。[方法]通过缺血缺氧无糖培养24 h构建心肌细胞损伤模型,利用5~40μmol/L的GS-Rb1与模型组细胞共同作用后,采用MTT和Annexin V-FITC/PI双染法检测细胞活性和凋亡率,荧光定量PCR法检测miR-21的表达,Western Blot法检测PDCD4蛋白的表达。[结果]GS-Rb1呈剂量依赖性保护心肌细胞,细胞活性由模型组的25.7%上升至53.3%。流式分析表明GS-Rb1使缺血缺氧造成的心肌细胞凋亡率由81.5%下降至31.0%;miR-21在模型组的表达下降了36.4%,GS-Rb1可以抑制miR-21的表达下降;在模型组中,PDCD4蛋白的表达上升了8.9倍,并可被GS-Rb1抑制。[结论]GS-Rb1可以减轻缺血缺氧引起的心肌细胞凋亡,并逆转了miR-21的下调及靶蛋白PDCD4的表达上调。
[Objective] To investigate the role of microRNA-21 (miR-21) and its target protein PDCD4 in the protective effect of ginsenoside Rb1 (GS-Rb1) on myocardial cells injured by hypoxia and hypoxia. [Method] The model of myocardial cell injury was established by hypoxia-ischemia and sugar-free culture for 24 h. MTT assay and Annexin V-FITC / PI double staining method were used to detect the effect of GS-Rb1 in 5-40 μmol / The cell viability and apoptotic rate were detected by real-time PCR. The expression of miR-21 was detected by real-time quantitative PCR. The expression of PDCD4 protein was detected by Western Blot. [Result] GS-Rb1 could protect cardiomyocytes in a dose-dependent manner, and the cell viability increased from 25.7% to 53.3% in the model group. Flow cytometry analysis showed that GS-Rb1 decreased the apoptotic rate of cardiomyocytes from 81.5% to 31.0% due to hypoxia-ischemia; miR-21 decreased 36.4% in model group and GS-Rb1 inhibited the expression of miR-21 Decreased; in the model group, the expression of PDCD4 protein increased 8.9 times, and can be GS-Rb1 inhibition. [Conclusion] GS-Rb1 can attenuate cardiomyocyte apoptosis induced by hypoxia and hypoxia, and reverse the down-regulation of miR-21 and the up-regulation of PDCD4.