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作 者:朱海燕[1,2] 王宇光[2] 马增春[2] 汤响林[2] 谭洪玲[2] 肖成荣[2] 陈志武[1] 高月[2]
机构地区:[1]安徽医科大学基础医学院药理学教研室,合肥230032 [2]军事医学科学院放射与辐射医学研究所,北京100850
出 处:《中药药理与临床》2017年第1期41-45,共5页Pharmacology and Clinics of Chinese Materia Medica
基 金:国家重点基础研究发展计划(973计划)资助项目(NO 2012CB518402)
摘 要:目的:观察丹参酮ⅡA(Tan ⅡA)对人脐静脉内皮细胞氧化损伤所致凋亡的保护作用机制研究。方法:不同浓度的丹参酮ⅡA预处理细胞24 h再给与4×10-4mol/L H_2O_2处理3 h。CCK-8法检测细胞活力;流式细胞术检测凋亡,ROS和线粒体膜电位值;高内涵筛选技术检测AIF;Cell Death Detection ELISA试剂盒检测DNA fragment。结果:丹参酮ⅡA(5、10、20×10-6mol/L)可以浓度依赖性的抑制H_2O_2诱导的内皮细胞损伤,TanI IA抑制H_2O_2引起的细胞凋亡降低被升高的ROS值,升高H_2O_2抑制的线粒体膜电位。同时可以抑制H_2O_2诱导的AIF的核转移并且H_2O_2引起的DNA fragment具有减轻作用。结论:丹参酮ⅡA可以减轻H_2O_2诱导的内皮细胞氧化损伤及凋亡,并且主要是通过抑制AIF核内转移实现的。Objective: To investigate the protective effect of Tan ⅡA on H2O2-induced oxidative stress injury and apoptosis in endothelial cells.Methods: HUVECs cells were pretreated with different concentrations of Tan ⅡA( 5,10,20 × 10-6mol/L) for 24 h,then treated with 4 ×10-4mol/L H2O2 for another 3 h.The percentage of cell viability was evaluated by cell counting kit-8( CCK-8) assay kit.Intracellular apoptosis,ROS and mitochondrial membrane potential( MMP) production were measured by flow cytometry.High-throughput screening technology was used to detect translocation change of AIF.Cell Death Detection ELISA was used to measure DNA fragment.Results: Our experimental studies demonstrated that Tan ⅡA concentrate-depended prevented H2O2-induced cell injury,decreased the production of H2O2-induced ROS and apoptosis,elevating H2O2 suppressed mitochondrial membrane potential( MMP) production.Furthermore,Tan ⅡA attenuated translocation of AIF induced by H2O2.Finally,Tan ⅡA depressed H2O2-induced DNA fragments.Conclusion: Tan ⅡA attenuateed H2O2-induced oxidative injury and apoptosis in endothelial cell.
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