目的 探讨京尼平对缺氧/复氧(H/R)损伤后大鼠心肌细胞凋亡及自噬的影响。 方法 建立H/R损伤模型，体外培养的大鼠H9c2心肌细胞行缺氧12 h、复氧4 h。实验分为对照组（Con）、京尼平组(GE)、缺氧/复氧组(H/R)、缺氧/复氧+京尼平组(H/R+GE)。细胞计数试剂盒-8（CCK-8）检测细胞存活率，流式细胞仪检测细胞凋亡，透射电子显微镜观察自噬体，Western blotting检测Bax、Bcl-2、P62、Beclin1、LC3-Ⅱ、蛋白激酶B(Akt)、p-Akt、哺乳动物雷帕霉素靶蛋白（mTOR）和p-mTOR蛋白的表达。 结果 京尼平预处理增强了H/R损伤后的H9c2心肌细胞活力,抑制细胞凋亡及自噬体累积，降低自噬结构断面积与细胞质断面积的比值。Western blotting结果显示，京尼平预处理减少了H/R损伤后Bax、LC3-Ⅱ和Beclin1蛋白表达，增加Bcl-2、P62、p-Akt和p-mTOR蛋白表达。 结论 京尼平可以抑制H/R损伤后心肌细胞凋亡及自噬，其机制可能与上调Akt/mTOR信号通路有关。

Objective  To investigate the effect of genipin on cardiomyocyte apoptosis and autophagy in rat after hypoxia/reoxygenation (H/R) injury.   Methods  The method  with hypoxia treatment of H9c2 cells for 12 hours and then reoxygenation treatment for 4 hours was used in the present study in order to establish H/R model. The H9c2 cells were divided into control group (Con), genipin group (GE), model group (H/R), model + genipin group (H/R+ GE). Cell viability was detected by cell counting kit-8(CCK-8). Cell apoptosis was determined by flow cytometry. Transmission electron microscopy was used to observe autophagosomes. The expression of Bax, Bcl-2, P62, Beclin1, LC3-Ⅱ, protein kinase B(Akt), p-Akt, mammalian target of rapamycin(mTOR), p-mTOR proteins were assessed by Western blotting.   Results Genipin pretreatment enhanced the cell viability, prevented cell apoptosis and autophagosome accumulation, and reduced the ratio of the cross-sectional areas of the autophagic structures to that of the cytoplasm after H/R injury in H9c2 cells. Western blotting showed that genipin pretreatment decreased the expression of Bax, LC3-Ⅱ, Beclin1 proteins and increased the expression of Bcl-2, p62, p-Akt, p-mTOR proteins after H/R injury.   Conclusion Genipin can inhibit H/R injury-induced apoptosis and autophagy, which may be through activating Akt/mTOR signaling pathway.