基础医学与临床 ›› 2021, Vol. 41 ›› Issue (10): 1451-1456.

• 研究论文 • 上一篇    下一篇

丁苯酞减轻H2O2诱导的人脐静脉和脐动脉内皮细胞氧化损伤

杨晓丽1*, 王征2, 张艳茹3, 冀静静3, 王孟帅4   

  1. 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
  • 收稿日期:2020-11-17 修回日期:2021-04-15 发布日期:2021-09-29
  • 通讯作者: *hbyxl@126.com
  • 基金资助:
    河北省卫健委青年科技课题(20200585)

Dl-3-n-butylphthalide attenuates H2O2-induced oxidative damage of human umbilical vein and umbilical artery endothelial cells

YANG Xiao-li1*, WANG Zheng2, ZHANG Yan-ru3, JI Jing-jing3, WANG Meng-shuai4   

  1. 1. Department of Neurology, the Affiliated Hospital of Hebei Engineering University, Handan 056002;
    2. Department of Critical Care Medicine, the First Hospital of Handan, Handan 056002;
    3. Department of Endocrinology, the Second Hospital of Handan, Handan 056001;
    4. Department of Neurology, the Second Hospital of Handan, Handan 056001, China
  • Received:2020-11-17 Revised:2021-04-15 Published:2021-09-29
  • Contact: *hbyxl@126.com

摘要: 目的 探讨丁苯酞(NBP)对过氧化氢(H2O2)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H2O2剂量建立两种细胞的氧化应激损伤模型。在加入H2O2前2 h,分别用两种剂量的丁苯酞(5和10 μmol/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 H2O2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H2O2诱导的上述变化。结论 丁苯酞可通过减轻H2O2造成的氧化损伤来保护血管内皮细胞。

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

Abstract: Objective To investigate the protective effect and mechanism of dl-3-n-butylphthalide (NBP) on hydrogen peroxide (H2O2) - 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 H2O2 for establishment of oxidative stress injury model. Then the cells were pre-incubated with two different dosages of NBP (5 and 10 μmol/L) 2 h before exposure to H2O2. 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 H2O2-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 H2O2. Conclusions NBP protects vascular endothelial cells by alleviating the oxidative damage induced by H2O2.

Key words: oxidative stress, dl-3-n-butylphthalide, human umbilical vein endothelial cells, human umbilical artery endothelial cells

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