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作 者:高琳琳[1] 李福荣[1] 康莉[1] 司艳红[1] 胡维诚[2]
机构地区:[1]泰山医学院病理生理学教研室,山东省泰安市271000 [2]山东大学医学院病理生理学教研室,山东省济南市250012
出 处:《中国动脉硬化杂志》2008年第9期689-692,共4页Chinese Journal of Arteriosclerosis
基 金:山东省卫生厅青年项目基金(JZ43)资助;山东省泰安市科技局科技基金(20051011)资助
摘 要:目的研究中药蚤休皂苷对H2O2诱导的脐静脉内皮细胞ECV304损伤的保护作用及其机制。方法体外培养ECV304,建立氧化损伤细胞模型,然后分为五个实验处理组:正常对照组、氧化损伤组、高浓度蚤休皂苷组、中浓度蚤休皂苷组和低浓度蚤休皂苷组,采用四甲基偶氮唑盐比色法检测蚤休皂苷对H2O2诱导的内皮细胞氧化损伤的影响,逆转录聚合酶链反应检测细胞间细胞粘附分子1和血管细胞粘附分子1mRNA的表达水平,流式细胞术定量检测细胞间细胞粘附分子1和血管细胞粘附分子1的表达。结果损伤后细胞吸光度值低于正常对照组(P<0.01),药物预处理后吸光度值增加,高浓度蚤休皂苷组吸光度值与正常组相比差异无显著性;药物预处理氧化损伤后,细胞间细胞粘附分子1和血管细胞粘附分子1mRNA的表达水平与损伤组相比明显减弱(P<0.01);损伤组中与内参照的灰度值之比最大,与正常组相比差异显著(P<0.01);损伤组中表达细胞间细胞粘附分子1和血管细胞粘附分子1的阳性细胞数增多,与正常组相比差异显著(P<0.01);药物预处理氧化损伤后,阳性细胞数明显减少,且此效应呈剂量依赖性(P<0.01)。结论蚤休皂苷可以保护H2O2造成的人脐静脉内皮细胞的氧化损伤,是通过抑制内皮细胞粘附分子的表达从而抑制炎症性损伤,达到保护内皮细胞、抗动脉粥样硬化的目的。Aim To study the mechanism of anti-injury of pariphyllin on the human umbiliar vein endothelial cell (hUVEC) ECV 304 induced by hydrogen peroxide (H2O2). Methods A model of endothelial cell oxidative damage induced into H2O2 was established, then cells were divided into five experimental groups including normal group, oxidative damage group and three different concertration pariphyllin groups. MTT assay was used to detect the protection of pariphyllin, reverse transcription-polymerase chain reaction (RT-PCR) were used to detect the mRNA expression level of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1), flow cytometry (FCM) was used to quantitate the expression of ICAM-1 and VCAM-1. Results Cell optical density in oxidation damaged group was lower than nomal control (P〈0.01); when pretreated by the medicine, the OD value was increased, and it had no significant difference in the high density pariphyllin than normal control (P〉0.05). The mRNA expression of ICAM-1and VCAM-1 was significantly descended (P〈0.01) in medicine treatment groups than in H2O2 damage group, FCM result discovered that the numbers of masculine cells which express ICAM-1 or VCAM-1 were obviously more than other groups (P〈0.01), but pretreated group could make the number lower and the effection was dose dependent. Conclusions Pariphyllin has the protective action on oxidative damage of ECV304, which was related to stabilizing the cell wall to inhibit the inflammatory reaction induced by ICAM-1 and VCAM-1, and then protect endothelial cell, prevent atherosclerosis.
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