[1]金鑫,易龙,陈春烨,等.膜电位及MAPK磷酸化在飞燕草素抑制Ox-LDL诱导的血管内皮细胞氧化损伤中的作用[J].第三军医大学学报,2009,31(19):1854-1858.
 JIN Xin,YI Long,CHEN Chun-ye,et al.Delphinidin-3-glucoside inhibits Ox-LDL-induced injury in vascular endothelial cells: roles of membrane potential and MAPK phosphorylation[J].J Third Mil Med Univ,2009,31(19):1854-1858.
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膜电位及MAPK磷酸化在飞燕草素抑制Ox-LDL诱导的血管内皮细胞氧化损伤中的作用(/HTML )
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《第三军医大学学报》[ISSN:1000-5404/CN:51-1095/R]

卷:
31卷
期数:
2009年第19期
页码:
1854-1858
栏目:
论著
出版日期:
2009-10-15

文章信息/Info

Title:
Delphinidin-3-glucoside inhibits Ox-LDL-induced injury in vascular endothelial cells: roles of membrane potential and MAPK phosphorylation
作者:
金鑫易龙陈春烨糜漫天
第三军医大学军事预防医学院营养与食品卫生学教研室,营养与食品安全重点实验室,重庆市医学营养研究中心
Author(s):
JIN Xin YI Long CHEN Chun-ye MI Man-tian
Department of Nutrition and Food Hygiene,  Chongqing Key Laboratory of Nutrition and Food Safety, Chongqing Medical Nutrition Research Center, College of Military Preventive Medicine, Third Military Medical University, Chongqing 400038, China
关键词:
飞燕草素葡萄糖苷动脉粥样硬化氧化低密度脂蛋白血管内皮细胞膜电位p38MAPK
Keywords:
delphinidin-3-glucoside atherosclerosis oxidized low density lipoprotein vascular endothelial cells membrane potential p38MAPK
分类号:
R151.3;R322.12;R329.25
文献标志码:
A
摘要:
目的   观察飞燕草素(Delphinidin-3-glucoside,Dp-3-glc)对氧化低密度脂蛋白(Ox-LDL)诱导的血管内皮细胞株EA.hy926的氧化应激损伤、细胞膜电位和线粒体膜电位改变及p38MAPK磷酸化的影响,探讨其抑制内皮细胞氧化应激的分子机制。   方法   不同浓度(25、50、100、200 μmol/L)的Dp-3-glc预处理内皮细胞2 h后,Ox-LDL(100 μg/ml)继续处理24 h,MTT法检测细胞活力;细胞培养上清液LDH、NO、MDA水平及细胞匀浆SOD酶活性采用试剂盒分别检测;荧光探针DCFH-DA标记细胞内活性氧(ROS)、膜电位敏感的阳离子荧光探针DiSC3(5)和阴离子荧光探针DiBAC4(3)分别标记细胞膜电位,罗丹明-123标记线粒体膜电位,激光共聚焦显微镜分别检测荧光强度;Western blot法检测细胞内p38MAPK的磷酸化水平。   结果   Dp-3-glc能明显抑制Ox-LDL诱导的内皮细胞MDA和LDH生成增加、NO分泌减少及细胞内SOD酶活力降低,并显著减少细胞内活性氧(ROS)生成。实验发现Ox-LDL能明显诱导细胞膜电位升高和线粒体膜电位下降,及增强膜电位相关的p38MAPK的磷酸化水平,而Dp-3-glc预处理能明显减弱Ox-LDL诱导的膜电位改变,并抑制p38MAPK的磷酸化。   结论   Dp-3-glc可能通过影响细胞膜电位、线粒体膜电位及膜电位相关的p38MAPK的磷酸化水平,削弱Ox-LDL诱导的内皮细胞氧化应激损伤。
Abstract:
Objective   To investigate the effects of delphinidin-3-glucoside (Dp-3-glc) on the oxidized injury, alteration of membrane potential and mitochondria potential, and p38MAPK phosphorylation of vascular endothelial cell line EA.hy926 induced by oxidized low density lipoprotein (Ox-LDL) and explore the molecular mechanism of the inhibitory effect of Dp-3-glc on endothelial oxidized injury.    Methods   Endothelial cells were preincubated for 2 h with Dp-3-glc at the concentrations of 25, 50, 100 or 200 μmol/L  and then treated for another 24 h with Ox-LDL of 100 μg/ml. MTT assay was used to detect the cell viability. MDA, LDH and NO in the supernatant and intracellular SOD activity were determined by the corresponding detection assay kits. Intracellular reactive oxygen species (ROS) production marked by DCFH-DA, membrane potential marked by DiSC3(5) and DiBAC4(3) and mitochondria potential marked by rhodamine-123 were respectively measured by laser confocal scanning microscopy. The phosphorylation level of p38MAPK was determined by Western blot assay.    Results   Preincubation with Dp-3-glc significantly inhibited Ox-LDL-induced reduction of cell viability, increase of MDA and LDH production, decrease of NO release and SOD activity, and intracellular ROS production in the endothelial cells. Ox-LDL obviously elevated the membrane potential, declined the mitochondria potential and increased the p38MAPK phosphorylation, while preincubation with Dp-3-glc inhibited the effects of Ox-LDL.    Conclusion   Dp-3-glc attenuates the Ox-LDL-induced stress injury in endothelial cells through decreasing the membrane potential and suppressing p38MAPK phosphorylation.

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更新日期/Last Update: 2009-09-29