野黄芩苷对缺氧缺糖损伤神经元的保护作用及机制研究
Protective effect and mechanisms of Scu on OGD injured neurons
目的：考察灯盏细辛中野黄芩苷对缺氧缺糖（oxygen glucose deprivation ,OGD）损伤神经元的保护作用和机制。方法：体外培养大鼠大脑皮层神经元，建立缺氧缺糖损伤模型，野黄芩苷（Scutellarinon，Scu）进行干预后，高效液相色谱法检测谷氨酸的释放、酶标仪检测钙离子浓度及线粒体膜电位的变化。结果：缺氧缺糖培养条件下，与对照组比较，模型组中谷氨酸、钙离子释放量均明显升高（p＜0.01），与模型组比较，Scu 12.5﹑25、50μg/ml组均不同程度降低了谷氨酸和钙离子（Ca2+）的释放量；与对照组比较，模型组中线粒体膜电位明显降低（p＜0.01），与模型组比较，Scu 25、50、100μg/ml组均不同程度的使线粒体膜电位升高。结论：野黄芩苷能抑制缺氧缺糖损伤神经元谷氨酸释放、抑制细胞内钙超载、升高线粒体膜电位等，对缺氧缺糖损伤的神经元有保护作用。
o investigate the effect and mechanisms of scutellarinon on neurons injured by OGD.Methods: Establish OGD model, after intervention by Scu, HPLC detected glutamic acid,the Reader detect the concentration of Calcium,and kit detected the changes of mitochondrial membrane potential. Results: 1 undering OGD culture conditions, compared with the control group, the release of glutamate and calcium in model group were significantly increased (P<0.01), compared with model group, the release of glutamate and calcium ions in Scu 12.5,25, 50 μg / ml Groups were reduced; with the control group, mitochondrial membrane potential significantly decreased in model group (P<0.01), compared with model group, the mitochondrial membrane potential increased in Scu12.5,25, 50μg / ml groups. Conclusion: Scu can inhibit the release of glutamate and the overload of calcium , furthermore it can increase mitochondrial membrane potential.So Scu has protective effect on OGD injury in neurons.
胡利民、史芳
基础医学神经病学、精神病学药学
野黄芩苷神经元缺氧缺糖损伤脑保护作用
ScutellarinneuronOxygen-glueose deprivation injury modelBrian protection
胡利民,史芳.野黄芩苷对缺氧缺糖损伤神经元的保护作用及机制研究[EB/OL].(2011-07-05)[2025-08-16].http://www.paper.edu.cn/releasepaper/content/201107-39.点此复制
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