• 首页期刊简介编委会刊物订阅专栏专刊电子刊学术动态联系我们English
引用本文:姜松国,徐磊,柴冬梅,朱辉武,林铮.石杉碱甲保护人脑微血管内皮细胞损伤的体外实验研究[J].中国现代应用药学,2015,32(3):277-281.
JIANG Songguo,XU Lei,CHAI Dongmei,ZHU Huiwu,LIN Zheng.Protect Effects of Huperzine A on Methylglyoxal Induced Injury in the Cultured Human Brain Microvascular Endothelial Cell in Vitro Experimental Study[J].Chin J Mod Appl Pharm(中国现代应用药学),2015,32(3):277-281.
【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 2177次   下载 1546 本文二维码信息
码上扫一扫!
分享到: 微信 更多
石杉碱甲保护人脑微血管内皮细胞损伤的体外实验研究
姜松国1, 徐磊2, 柴冬梅3, 朱辉武1, 林铮2
1.浙江省江山市第四人民医院,浙江 江山 324100;2.浙江大学医学院附属第二医院,杭州 310009;3.浙江省江山市上余镇卫生院,浙江 江山 324123
摘要:
目的 体外实验研究石杉碱甲对人脑微血管内皮细胞(human brain microvascular endothelial cells,HBMEC)损伤的保护作用和机制。方法 在培养的HBMEC上,利用丙酮醛诱导细胞损伤,通过MTT检测细胞活力,LDH、SOD活性试剂盒及caspase-3活性试剂盒检测细胞损伤情况,观察石杉碱甲的作用和机制。结果 石杉碱甲呈浓度依赖地保护MGO诱导的细胞损伤,在10-5 mol?L-1时呈最大保护作用。丙酮醛能诱导HBMEC的SOD活性下降,而石杉碱甲(10-6,10-5 mol?L-1)能逆转这种作用。进一步研究发现石杉碱甲能抑制丙酮醛诱导的caspase-3活性上升。结论 石杉碱甲对丙酮醛诱导的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:  石杉碱甲  脑微血管内皮细胞  丙酮醛  凋亡
DOI:
分类号:
基金项目:浙江省自然科学基金(Y2100294);浙江省卫生厅项目(2011KYA073,2014KYA100);浙江省中医药项目(2014ZA067)
Protect Effects of Huperzine A on Methylglyoxal Induced Injury in the Cultured Human Brain Microvascular Endothelial Cell in Vitro Experimental Study
JIANG Songguo1, XU Lei2, CHAI Dongmei3, ZHU Huiwu1, LIN Zheng2
1.The Fourth People’s Hospital of Jiangshan, Jiangshan 324100, China;2.The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310009, China;3.The Rural Hospital of Shangyu Town, Jiangshan 324123, China
Abstract:
OBJECTIVE To evaluate the effects of huperzine A on the methylglyoxal (MGO) induced injury in the cultured human brain microvascular endothelial cell (HBMEC). METHODS HBMEC cell line was chosen to induce MGO injury. Cell vitality was measured by using MTT, LDH release, SOD activity were tested by kits. Cell apoptosis was measured by caspase 3 activity. RESULTS Huperzine A dose-dependently protected MGO induced HBMEC injury. At 10-5 mol?L-1 of huperzine A manifested the maximum effects. MGO increased SOD activity, which were reversed by pretreatment of venlafaxine (10-6 and 10-5 mol?L-1). Furthermore, huperzine A (10-6 and 10-5 mol?L-1) also decreased MGO induced caspase 3 activity increasing. CONCLUSION Huperzine A protected MGO induced injury in the cultured HBMEC, which may be involved its anti-oxidation and anti-apoptosis activity.
Key words:  huperzine A  human brain microvascular endothelial cell  methylglyoxal  apoptosis
扫一扫关注本刊微信