目的 探讨 miRNA⁃155 在缺糖缺氧心肌细胞模型中对 Notch 信号通路及心肌细胞凋亡与自 噬的影响。方法 建立缺糖缺氧细胞（oxygen⁃glucose deprivation，OGD）模型，细胞分为正常对照组，OGD 组，OGD 组 + miRNA⁃155 inhibitor 阴性对照组及 OGD 组+ miRNA⁃155 inhibitor 组。利用 RT⁃qPCR 检测模型 组与正常对照组心肌细胞中 miRNA⁃155 的表达情况；利用 Western blot 检测正常对照组，OGD 组，OGD 组 + miRNA⁃155 抑制剂阴性对照组及 OGD 组+ miRNA⁃155 抑制剂组中 Notch1，HES1，Beclin1 及 Caspase⁃3 的 表达情况；利用 CCK⁃8 实验检测各组心肌细胞的活性。结果 RT⁃qPCR 结果显示，与正常对照组相比较， 模型组心肌细胞中 miRNA⁃155 的表达显著升高；Western blot 结果显示，抑制 miRNA⁃155 的表达后，可显著 升高缺糖缺氧心肌细胞中 Notch1，HES1，Beclin1 的表达，降低细胞中 Caspase⁃3 的表达；CCK⁃8 实验结果显 示，抑制 miRNA⁃155 的表达后，可显著提高缺糖缺氧心肌细胞的活性。结论 MiRNA⁃155 inhibitor 可通过 提高 Notch1 及 HES1 的表达，促进 Notch 信号通路激活，促进细胞自噬，抑制细胞凋亡，提高心肌细胞的活

Objective To investigate the effect of miRNA ⁃ 155 on autophagy and apoptosis of myocardial cells and Notch signaling pathway in oxygen ⁃glucose deprivation model. Methods Establishing the model of oxygen⁃glucose deprivation（OGD），the cells were divided into normal control group，OGD group，OGD + miRNA⁃ 155 inhibitor negative control group and OGD + miRNA⁃155 inhibitor group. RT⁃qPCR was used to detect the expression of miRNA ⁃155 in myocardial cells in the OGD group and the normal control group. The expression of Notch1，Hes1，Beclin1 and Caspase ⁃3 in OGD group，OGD + miRNA ⁃155 inhibitor negative control group and OGD+ miRNA ⁃155 inhibitor group was detected by Western blots. The activity of myocardial cells in each group was detected by the CCK⁃8 assay. Results The result of RT⁃qPCR showed that the expression of miRNA⁃155 was significantly increased in OGD group，compared with normal control group. The results of Western blots showed that miRNA ⁃155 inhibitor significantly increased the expression of Notch1，HES1，Beclin1 and decreased the expression of Caspase⁃3 in myocardial cells with oxygen⁃glucose deprivation. The results of CCK⁃8 showed that inhi⁃ bition the expression of miRNA⁃155 could significantly increase the activity of myocardial cells with oxygen⁃glucose deprivation. Conclusion MiRNA⁃155 inhibitor exerts the myocardial protection through enhancing the expression of Notch1 and HES1，activating Notch signaling pathway，promoting autophagy，inhibitting apoptosis and increase