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作 者:王晓东[1] 陈美苑[2] 曾志[3] 周卓妍[2] 杨默[4]
机构地区:[1]暨南大学附属第一医院神经外科,广东广州510632 [2]暨南大学医学院生理学系,广东广州510632 [3]广东药学院生理学系,广东广州510006 [4]南方医科大学南方医院血液科,广东广州510515
出 处:《中国病理生理杂志》2015年第3期409-414,共6页Chinese Journal of Pathophysiology
基 金:国家自然科学基金资助项目(No.81270580)
摘 要: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(P<0.01);与对照组比较,Co Cl2组的细胞凋亡率明显升高(P<0.05),而Co Cl2+TPO组的细胞凋亡率显著低于Co Cl2组(P<0.05);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(P<0.01)。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。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 chan-ges of the mitochondrial membrane potential ( MMT) were determined by flow cytometry and fluorescence microscopy.RE-SULTS: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.
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