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目的:研究清开灵对小鼠脑微血管内皮细胞缺氧损伤MLCK基因转录的影响。方法:细胞分为正常对照组(有糖Earle液)、模型组(缺氧缺糖模拟缺血:无糖Earle液,37℃,5%CO2,1%O2培养24 h)、清开灵低、中、高浓度组(缺氧缺塘+清开灵1%、2%、4%),在37℃、5%CO2培养箱中培养24 h后经MTT比色法检测细胞活力、荧光定时定量PCR检测MLCK基因转录。结果:缺氧缺糖24 h后微血管内皮细胞活性降低(P<0.05)、MLCK基因转录被抑制(P<0.05);清开灵1%、2%、4%组均抑制了缺糖缺氧条件下微血管内皮细胞活性的降低(P<0.05),清开灵4%组降低MLCK的表达(P<0.05)。结论:缺糖缺氧条件下微血管内皮细胞活性降低。清开灵通过抑制MLCK的表达,恢复BBB的部分屏障功能。
Objective: To investigate the effect of Qingkailing on MLCK gene transcription in mouse brain microvascular endothelial cell (HUVEC) induced by hypoxia. Methods: The cells were divided into normal control group (Earle fluid with sugar), model group (hypoxic-ischemic-mock-simulated ischemia: earle-free solution, 37 ℃, 5% CO2, 1% O2 for 24 h) , Medium and high concentration group (hypoxia deficiency pond + Qingkailing 1%, 2%, 4%), cultured in 37 ℃, 5% CO 2 incubator for 24 hours, MTT assay cell viability, fluorescence timing Quantitative PCR detection of MLCK gene transcription. Results: The activity of microvascular endothelial cells was decreased 24 h after hypoxia-glucose deprivation (P <0.05), and MLCK gene transcription was inhibited (P <0.05). Qingkailing 1%, 2% and 4% (P <0.05), and 4% Qingkailing decreased the expression of MLCK (P <0.05). Conclusion: The activity of microvascular endothelial cells in hypoglycemic and hypoxia conditions is decreased. Qingkailing restores part of the BBB barrier function by inhibiting the expression of MLCK.