地西泮对缺血再灌注损伤过程中氨基酸和自由基含量的影响

B Hu, Y Mei, G Wei, X Qiu, S Sun, E Tong
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引用次数: 0

摘要

研究了地西泮在脑缺血和再灌注过程中对缺血神经元的保护作用及其机制。将 63 只 Wistar 大鼠随机分为 9 组:对照组(n = 7);缺血(is)组,包括 is3 h、is3 h/rep1-h、is3 h/rep2-h、is3 h/rep3-h(每组 n = 7);地西泮治疗组(10 mg/kg,i.p.),包括 is3-h、is3-h/rep1-h、is3-h/rep2-h、is3-h/rep3-h 亚组(每组 n = 7)与玉米螟大脑中动脉闭塞动物模型。缺血组与地西泮处理组比较发现,地西泮能明显减少谷氨酸、天冬氨酸、MDA的产生,增加GABA、SOD和GSH-PX的合成和释放。结论地西泮通过调节兴奋/抑制性氨基酸和自由基的合成与释放的复杂机制对神经元发挥保护作用。
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Effect of diazepam on the contents of amino acids and free radical during ischemia/reperfusion injury.

The protective effect and mechanism of diazepam on ischemia neurons during cerebral ischemia and reperfusion were studied. Sixty-three Wistar rats were divided randomly into nine groups: control group (n = 7), ischemia (is) groups including subgroups of is3 h, is3-h/rep1-h, is3-h/rep2-h, is3-h/rep3-h(n = 7 in each group), diazepam treated groups (10 mg/kg, i.p.), including subgroups of is3-h, is3-h/rep1-h, is3-h/rep2-h, is3-h/rep3-h (n = 7 in each group) with Zea longa's animal model of middle cerebral artery occlusion. The comparison between the ischemia group and diazepam-treated group showed that diazepam could obviously decrease the production of glutamate, asparate, MDA and increase the synthesis and release of GABA, SOD and GSH-PX. It was concluded that diazepam exerted its protective effects on neurons through complex mechanisms of regulating the synthesis and release of excitotary/inhibitory amino acids and free radicals.

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