促血小板生成素对化学性缺氧诱导的PC12细胞凋亡的影响

目的:研究促血小板生成素(TPO)对化学性缺氧诱导的大鼠嗜铬细胞瘤PC12细胞凋亡的影响及保护作用。方法:将PC12细胞进行相应实验处理,分为对照组、氯化钴(Co Cl2)处理组、Co Cl2+TPO组及TPO对照组。检测各组PC12细胞的存活率并用Annexin V/PI双染流式细胞术分别检测细胞凋亡率,线粒体膜电位的变化及细胞内活性氧簇的变化。结果:化学性缺氧模拟剂Co Cl2可以明显抑制PC12细胞的生长(P0.01);与对照组比较,Co Cl2组的细胞凋亡率明显升高(P0.05),而Co Cl2+TPO组的细胞凋亡率显著低于Co Cl2组(P0.05);TPO能减少细胞内活性氧簇生成以及抑制细胞线粒体膜电位的降低(P0.01)。结论:TPO能对抗Co Cl2缺氧所致的细胞凋亡,稳定线粒体膜电位,发挥细胞保护作用。

Effect of thrombopoietin on chemical hypoxia-induced apoptosis of PC12 cells

AIM: To study the effect of thrombopoietin (TPO) on chemical hypoxia-induced apoptosis of the Rattus norvegicus adrenal pheochromocytoma (PC12) cells. METHODS: The cultured PC12 cells were randomly divided into normal control group, cobalt chloride (CoCl₂) group, CoCl₂+TPO group and TPO group. The cell viability was mea-sured by MTT assay. The effect of TPO on CoCl₂-induced cell apoptosis was analyzed by flow cytometry with Annexin V/PI double staining. The intracellular reactive oxygen species (ROS) were detected by fluorescence microscopy, and the changes of the mitochondrial membrane potential (MMT) were determined by flow cytometry and fluorescence microscopy. RESULTS: Chemical oxygen agent CoCl₂ significantly inhibited the growth of PC12 cells (P<0.01). The apoptotic rate in CoCl₂ group was obviously higher than that in control group (P<0.05), while the apoptotic rate in CoCl₂+TPO group was obviously lower than that in CoCl₂ group (P<0.05). TPO decreased the production of ROS, and inhibited the decrease in MMP induced by CoCl₂ (P<0.01). CONCLUSION: TPO has a protective effect against CoCl₂-induced apoptosis of PC12 cells by decreasing the production of ROS and inhibiting the decrease in MMP.