【摘要】 目的:通过观察黄芩苷对体外无糖复合低氧致人脑微血管内皮细胞损伤的保护作用,探讨黄芩苷抗脑缺血的作用机制。方法:体外培养人脑微血管内皮细胞(HBMVEC),随机分为6组:空白对照组,模型组,黄芩苷高剂量组,黄芩苷中剂量组,黄芩苷低剂量组,尼莫地平组。利用试剂盒检测各组细胞的生存活性,乳酸脱氢酶(LDH)漏出率、钠钾-三磷酸腺苷酶(Na+-K+-ATPase)及钙-三磷酸腺苷酶(Ca2+-ATPase)活性及细胞内Ca2+。用流式细胞仪检测各组细胞的凋亡百分率。结果:与空白对照组比较,模型组细胞的存活率、Na+-K+-ATPase及Ca2+-ATPase活性均明显降低(P<0.05,P<0.01),而LDH的漏出率、细胞内Ca2+浓度及细胞的凋亡率则明显升高(P<0.01)。与模型组比较,黄芩苷高剂量组细胞的存活率、Na+-K+-ATPase及Ca2+-ATPase活性明显升高(P<0.05,P<0.01),而黄芩苷高剂量组的LDH的漏出率及细胞内Ca2+浓度则明显减低(P<0.05,P<0.01),且降低细胞内Ca2+的作用明显优于尼莫地平组。其中黄芩苷中剂量组与高剂量组细胞凋亡百分率明显降低(P<0.01)。结论:黄芩苷能明显提高体外无糖合并缺氧导致的人脑微血管内皮细胞的生存活性,其机制可能与其能够改善细胞的能量代谢,抑制细胞内钙超载,并进一步降低细胞凋亡有关。更多还原

【Abstract】 Objective:To investigate the mechanisms of baicalin on anti-cerebral ischemic through observing the effect of baicalin on human brain microvascular endothelial cell under the glucose deprivation combined with hypoxia condition.Methods:Human brain microvascular endothelial cells( HBMVECs) cultured in vitro were divided into the following groups:normal group,model group,baicalin high dose group,baicalin middle dose group,baicalin low dose group,nimodipine group.The kits were used to detect the cell viability,leakage rate of lactate dehydrigenase( LDH),Na+-K+-ATPase,Ca2+ -ATPase,the concentration of Ca2+ in each group, and apoptosis rates of each group were analyzed by flow cytometry( FCM).Results:Compared with the normal group,the cell viability, Na+-K+-ATPase and Ca2+ -ATPase in model group decreased significantly( P < 0.01,P < 0.05).But the leakage rate of LDH, Ca2+ in cells and apoptosis rates increased remarkably( P < 0.01).Compared with the model group,the cell viability,Na+-K+-ATPase and Ca2+ -ATPase increased obviously( P < 0.01,P < 0.05) in baicalin high dose group.But the leakage rate of LDH and Ca2+ in cells in baicalin high dose group decreased significantly comparing with that of model group( P < 0.05,P < 0.01).And the reduction of intracellular Ca2+ was superior to that of nimodipine group.Meanwhile,the apoptosis rates decreased significantly in both baicalin high and middle dose groups( P < 0.01).Conclusion:Baicalin could improve the cell viability of HBMVECs under the glucose deprivation combined with hypoxia condition.And the mechanisms were related with improving the energy metabolism,inhibiting intracellular calcium overload and decreasing the apoptosis rate of cells furtherly.更多还原