丁苯酞减轻H_(2)O_(2)诱导的人脐静脉和脐动脉内皮细胞氧化损伤  

Dl-3-n-butylphthalide attenuates H_(2)O_(2)-induced oxidative damage of human umbilical vein and umbilical artery endothelial cells

作　　者：杨晓丽 王征[2] 张艳茹 冀静静 王孟帅 YANG Xiao-li;WANG Zheng;ZHANG Yan-ru;JI Jing-jing;WANG Meng-shuai(Department of Neurology, the Affiliated Hospital of Hebei Engineering University, Handan 056002;Department of Critical Care Medicine,the First Hospital of Handan, Handan 056002;Department of Endocrinology, the Second Hospital of Handan, Handan 056001;Department of Neurology, the Second Hospital of Handan, Handan 056001, China)

机构地区：[1]河北工程大学附属医院神经内科,河北邯郸056002 [2]邯郸市第一医院重症医学科,河北邯郸056002 [3]邯郸市第二医院内分泌科,河北邯郸056001 [4]邯郸市第二医院神经内科,河北邯郸056001

出　　处：《基础医学与临床》2021年第10期1451-1456,共6页Basic and Clinical Medicine

基　　金：河北省卫健委青年科技课题(20200585)。

摘　　要：目的探讨丁苯酞(NBP)对过氧化氢(H_(2)O_(2))诱导的血管内皮细胞(人脐静脉和脐动脉)氧化损伤的保护作用及发生机制。方法体外培养人脐静脉内皮细胞(HUVECs)和人脐动脉内皮细胞(HUAECs)。用四甲基偶氮唑盐(MTT)法筛选合适的H_(2)O_(2)剂量建立两种细胞的氧化应激损伤模型。在加入H_(2)O_(2)前2 h,分别用两种剂量的丁苯酞(5和10μmol/L)预孵育细胞,用MTT法检测细胞活力,罗丹明123检测线粒体膜电位,Annexin V/PI双染法检测凋亡细胞,Fura-4/AM检测细胞内游离钙。结果H_(2)O_(2)刺激可导致HUVECs和HUAECs细胞活力下降,线粒体膜电位下降,细胞内游离钙增多,细胞凋亡率上升(P<0.05)。丁苯酞可改善H_(2)O_(2)诱导的上述变化。结论丁苯酞可通过减轻H_(2)O_(2)造成的氧化损伤来保护血管内皮细胞。Objective To investigate the protective effect and mechanism of dl-3-n-butylphthalide(NBP)on hydrogen peroxide(H_(2)O_(2))-induced oxidative damage of vascular endothelial cells(VECs).Methods Human umbilical vein endothelial cells(HUVECs)and human umbilical artery endothelial cells(HUAECs)were cultured and MTT assay was used to find the appropriate dosage of H_(2)O_(2) for establishment of oxidative stress injury model.Then the cells were pre-incubated with two different dosages of NBP(5 and 10μmol/L)2 h before exposure to H_(2)O_(2).The cell viability was detected by MTT assay,mitochondrial membrane potential was measured by rhodamine 123,cell apoptosis was detected by Annexin-V/PI double staining,and intracellular free Ca2+was measured by Fura-4/AM.Results H_(2)O_(2)-induced oxidative injury reduced the cell viability of HUVECs and HUAECs,increased the intracellular free Ca2+concentration thus leading to mitochondrial membrane potential decline and cell apoptosis(P<0.05).However,NBP treatment improved the above changes induced by H_(2)O_(2).Conclusions NBP protectsvascular endothelial cells by alleviating the oxidative damage induced by H_(2)O_(2).

关 键 词：氧化应激 丁苯酞 人脐静脉内皮细胞 人脐动脉内皮细胞 

分 类 号：R363[医药卫生—病理学]