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目的:研究葛根素对缺氧损伤的大鼠脑微血管内皮细胞(rCMEC)凋亡和功能的影响及其机制。方法:建立缺氧损伤的rCMEC模型,采用四甲基偶氮唑盐法(MTT),流式细胞术,酶联免疫吸附法(ELISA)和免疫印记法(Western blot),观察葛根素对rCMEC分泌组织型纤溶酶原激活物(t-PA),组织纤溶酶原激活物抑制剂(PAI),一氧化氮(NO),内皮素(ET),表达血管内皮生长因子(VEGF)和内皮型一氧化氮合酶(eNOS)的影响。结果:葛根素可以减轻缺氧损伤对rCMEC的影响,降低其凋亡率,可降低rCMEC胞内钙离子的浓度,提高VEGF和eNOS的表达,并显著提高t-PA/PAI和NO/ET的比值。结论:葛根素对缺氧损伤的脑微血管内皮细胞有保护作用,其机制可能与促进VEGF的表达,激活VEGF受体介导的下游通道有关。
Objective: To study the effect and mechanism of puerarin on apoptosis and function of rat brain microvascular endothelial cells (rCMEC) injured by hypoxia. Methods: The hypoxia-induced rCMEC model was established. MTT, flow cytometry, ELISA and Western blotting were used to observe the effect of puerarin on rCMEC Tissue plasminogen activator (t-PA), tissue plasminogen activator inhibitor (PAI), nitric oxide (NO), endothelin (ET), vascular endothelial growth factor Effect of endothelial nitric oxide synthase (eNOS). Results: Puerarin could reduce the effect of hypoxic injury on rCMEC and decrease its apoptosis rate, decrease the concentration of intracellular Ca2 + in rCMEC, increase the expression of VEGF and eNOS, and significantly increase the levels of t-PA / PAI and NO / ET ratio. CONCLUSION: Puerarin has a protective effect on hypoxia-injured brain microvascular endothelial cells. The mechanism may be related to the promotion of VEGF expression and activation of VEGF receptor-mediated downstream channels.