• 首页期刊简介编委会刊物订阅专栏专刊电子刊广告合作联系我们English
引用本文:姜松国,柴冬梅,朱辉武,林铮,戴海斌.氟西汀对丙酮醛诱导的人脑微血管内皮细胞损伤的保护作用[J].中国现代应用药学,2014,31(6):650-654.
JIANG Songguo,CHAI Dongmei,ZHU Huiwu,LIN Zheng,DAI Haibin.Effects of Fluoxetine on Methylglyoxal Induced Injury in the Cultured Human Brain Microvascular Endothelial Cells[J].Chin J Mod Appl Pharm(中国现代应用药学),2014,31(6):650-654.
【打印本页】   【HTML】   【下载PDF全文】   查看/发表评论  【EndNote】   【RefMan】   【BibTex】
←前一篇|后一篇→ 过刊浏览    高级检索
本文已被:浏览 2162次   下载 1211 本文二维码信息
码上扫一扫!
分享到: 微信 更多
氟西汀对丙酮醛诱导的人脑微血管内皮细胞损伤的保护作用
姜松国1, 柴冬梅2, 朱辉武1, 林铮3, 戴海斌3
1.浙江省江山市第四人民医院,浙江 江山 324100;2.浙江省江山市上余镇卫生院,浙江 江山 324123;3.浙江大学医学院附属第二医院,浙江 杭州310009
摘要:
目的 研究氟西汀对丙酮醛诱导的人脑微血管内皮细胞(HBMEC)损伤的保护作用。方法 在培养的HBMEC上,利用丙酮醛诱导的细胞损伤,通过MTT检测细胞活力,SOD、MDA试剂盒检测细胞的氧化活性,casepase 3活性试剂盒和流式细胞仪检测细胞凋亡,观察氟西汀的作用和机制。结果 氟西汀呈浓度依赖地保护丙酮醛(MGO)诱导的细胞损伤,在10-5 mol·L-1时呈最大保护作用。MGO能降低细胞上清SOD活性而升高MDA含量,而氟西汀(10-5 mol·L-1)能逆转这种作用,并能抑制MGO诱导的caspase-3活性上升和凋亡。结论 氟西汀对丙酮醛诱导的HBMEC的损伤具有保护作用,这可能与其抗自由基和抗凋亡作用有关。
关键词:  氟西汀  丙酮醛  凋亡  人脑微血管内皮细胞
DOI:
分类号:
基金项目:国家自然科学基金(81173040, 81373391, 81302747);浙江省科技厅项目(2010C33038);浙江省卫生厅项目(2011KYA065, 2011KY A073 , 2012RCA027);浙江省中医药项目(2012ZB091);浙江省教育厅项目(Y201328670)
Effects of Fluoxetine on Methylglyoxal Induced Injury in the Cultured Human Brain Microvascular Endothelial Cells
JIANG Songguo1, CHAI Dongmei2, ZHU Huiwu1, LIN Zheng3, DAI Haibin3
1.The Fourth People's Hospital of Jiangshan, Jiangshan 324100, China;2.The Rural Hospital of Shangyu Town, Jiangshan 324123, China;3.The Second Affiliated Hospital of Zhejiang University School of Medicine, Hangzhou 310009, China
Abstract:
OBJECTIVE To evaluate the effects of fluoxetine on the methylglyoxal(MGO) induced injury in the cultured human brain microvascular endothelial cells(HBMEC). METHODS In the cultured HBMEC, fluoxetine was added before MGO deprivation injury. Cell injury was measured by MTT, SOD activity and MDA content. Cell apoptosis was measured by caspase-3 activity and annexin V/PI formation. RESULTS Fluoxetine dose-dependently protected MGO induced HBMEC injury. Fluoxetine at 10-5 mol·L-1 manifested the maximum effects. MGO decreased SOD activity and increased MDA content, which were reversed by pretreatment of fluoxetine (10-5 mol·L-1). Furthermore, fluoxetine (10-5 mol·L-1) also decreased MGO induced caspase-3 activity increasing and annexin V/PI formation. CONCLUSION Fluoxetine protects MGO induced injury in the cultured HBMEC, which may be involved its anti-oxidation and anti-apoptosis activity.
Key words:  fluoxetine  methylglyoxal  apoptosis  human brain microvascular endothelial cells
扫一扫关注本刊微信