王冰, 马静, 王文, 王碧, 李锋, 肖茜, 王宗仁. 芪丹通脉片保护缺氧内皮细胞的实验研究[J]. 心脏杂志, 2009, 21(4): 493-495.
    引用本文: 王冰, 马静, 王文, 王碧, 李锋, 肖茜, 王宗仁. 芪丹通脉片保护缺氧内皮细胞的实验研究[J]. 心脏杂志, 2009, 21(4): 493-495.
    Protective effects of qidantongmai tablets on anoxic human umbilical vein endothelial cells[J]. Chinese Heart Journal, 2009, 21(4): 493-495.
    Citation: Protective effects of qidantongmai tablets on anoxic human umbilical vein endothelial cells[J]. Chinese Heart Journal, 2009, 21(4): 493-495.

    芪丹通脉片保护缺氧内皮细胞的实验研究

    Protective effects of qidantongmai tablets on anoxic human umbilical vein endothelial cells

    • 摘要: 目的 观察芪丹通脉片(QDTMT)对缺氧内皮细胞的保护机制。方法 原代培养、鉴定人脐静脉内皮细胞(HuVECs)。制备含QDTMT的血清并干预传代的HuVECs。将HuVECs根据不同处理因素随机分为 3 组:空白对照组、生理盐水组和QDTMT组,用流式细胞仪检测各组细胞的凋亡率。用免疫荧光染色法检测生理盐水组和QDTMT组细胞上血管内皮生长因子受体2(VEGFR2)的表达。结果 培养的HuVECs中具有特征性的短棒状细胞器Weible-Palade小体。流式细胞仪检测结果显示,与空白对照组相比,缺氧培养的HuVECs的凋亡率增加,但QDTMT组内皮细胞的凋亡率明显低于生理盐水组(P<0.05)。免疫荧光染色检测可见QDTMT组内皮细胞VEGFR2的表达强于生理盐水组。结论 QDTMT抗缺氧的HuVECs凋亡的作用可能与其促进VEGFR2的表达有关。

       

      Abstract: AIM: To explore the protective mechanisms of qidantongmai tablet (QDTMT) for anoxic human umbilical vein endothelial cells (HuVECs). METHODS: Cells were obtained from infant umbilical cord for primary cultivation and they were then identified by morphological character. The prepared serum of QDTMT was added to the passage of HuVEC. Endothelial cells were divided into three groups: normoxia control, normal saline and QDTMT group. The apoptosis rate of HuVECs was observed in flow cytometry (FCM) assay. Using immunofluorescence microscope, we examined the cellular distribution of VEGFR2 in hypoxic HuVECs. RESULTS: We found the characteristic Weible-Palade bodies under microscope in cultured HuVECs. FCM assay showed that the apoptosis rate of hypoxic HuVECs was higher than in normoxia control, whereas the apoptosis rate was higher in normal saline group than in QDTMT group (P<0.05). VEGFR2 expression level of HuVECs was higher in QDTMT group than in normal saline group. CONCLUSION: Under hypoxic condition, QDTMT may exert protective effects on anoxic HUVECs through enhancing VEGFR2 expression.

       

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