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首页> 外文期刊>Chinese Medical Journal >Protective effects of Ginkgo biloba extract on rats during cerebral ischemia/ reperfusion
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Protective effects of Ginkgo biloba extract on rats during cerebral ischemia/ reperfusion

机译:银杏叶提取物对大鼠脑缺血/再灌注的保护作用

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Objective To study the effect of Ginkgo biloba extract on rats during ischemia/reperfusion and its influence on intracellular calcium in hippocampal neurons. Methods Model of intraluminal occlusion of the middle cerebral artery (MCAO) was used to prepare the ischemia/reperfusion cortex tissue. Concentration of MDA was determined by measuring thiobarbituric acid-reactive substance. GSH-PX was quantified using the thiobarbituric acid (TBA) technique. SOD was assayed througha xanthine method. Endogenous amino acids were quantified by high performance liquid chromatographic (HPLC) analysis. Primary culturs of hippocampal neurons were prepared for a free intracelluiar calcium ([Ca~(2+)] I) assay by Fura-2 based single cell microfluoremetric technique. Results Comparing control and treatment groups, the concentration of SOD and GSH-PX were higher, whereas that of MDA was much lower; the concentration of glutamate and aspartate decreased and that of GABA increased markedly at all time point (P < 0.01), Gly also decreased at some time points (P< 0.05). The differences were significant between the groups of 10 mg/kg, 15 mg/kg and the groups of 5 mg/kg. When 1 x 10~(-5) mol/L glutamate was applied with 25 μg/ml ginkgo biloba extract to cultured neurons, the increase in [Ca~(2+)] I was lower than that caused by applying glutamate alone. Its peak value was much lower and increased phase was longer, its declining phase was shorter. After returning to baseline, the application of 1 x 10~(-5) mol/L glutamate could induce the reaction to recover. Conclusions Ginkgo biloba extract could protect damaged neurons by keeping the balance of inhibitory/ excitatory aminoacids, enhancing the free radical scavengers system, and inhibiting the effect of glutamate on [Ca~(2+)] I.
机译:目的研究银杏叶提取物对大鼠缺血/再灌注的影响及其对海马神经元细胞内钙的影响。方法采用大脑中动脉腔内闭塞(MCAO)模型制备缺血/再灌注皮质组织。通过测量硫代巴比妥酸反应性物质来确定MDA的浓度。 GSH-PX使用硫代巴比妥酸(TBA)技术进行定量。 SOD通过黄嘌呤法测定。内源氨基酸通过高效液相色谱(HPLC)分析进行定量。通过基于Fura-2的单细胞微荧光技术制备海马神经元的原代培养物,以进行游离细胞内钙([Ca〜(2+)] I)测定。结果与对照组和治疗组相比,SOD和GSH-PX的浓度较高,而MDA的浓度较低。谷氨酸和天门冬氨酸的浓度在所有时间点均下降,GABA的浓度在所有时间点均显着上升(P <0.01),Gly在某些时间点也下降(P <0.05)。 10 mg / kg,15 mg / kg组和5 mg / kg组之间的差异是显着的。当将1 x 10〜(-5)mol / L谷氨酸与25μg/ ml银杏叶提取物应用于培养的神经元时,[Ca〜(2+)] I的增加低于单独使用谷氨酸的结果。它的峰值要低得多,增加相的时间更长,下降相的时间更短。恢复到基线后,使用1 x 10〜(-5)mol / L谷氨酸可以诱导反应恢复。结论银杏叶提取物可通过保持抑制性/兴奋性氨基酸平衡,增强自由基清除剂系统和抑制谷氨酸对[Ca〜(2+)] I的作用来保护受损的神经元。

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