不同脑温状态下银杏叶提取物对大鼠缺血脑组织氨基酸及自由基的影响

Influence of Ginkgo biloba extract on amino acids and free radical in ischemic cerebral tissue under different cerebral temperature in rats

目的探讨不同脑温状态下银杏叶提取物(GBE)对大鼠缺血脑组织谷氨酸(Glu)、γ-氨基丁酸(GABA)、超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)、丙二醛(MDA)的影响。方法建立大鼠大脑中动脉缺血再灌注模型,将大鼠随机分为常温假手术组、常温脑缺血组、亚低温脑缺血组、常温银杏叶组、轻度高温银杏叶组、亚低温银杏叶组,诱导目标脑温,测定各组缺血脑组织Glu、GABA、SOD、GSH-Px、MDA含量。结果与常温假手术组比较,常温脑缺血组及轻度高温银杏叶组、常温银杏叶组Glu、GABA、MDA水平均显著增高,SOD、GSH-Px水平均显著降低。与常温脑缺血组比较,常温银杏叶组、亚低温脑缺血组及亚低温银杏叶组Glu、MDA水平均显著降低,GABA、SOD、GSH-Px水平均显著增高。与常温银杏叶组比较,轻度高温银杏叶组Glu、MDA水平均显著增高,GABA、SOD、GSH-Px水平均显著降低;亚低温脑缺血组及亚低温银杏叶组Glu、MDA水平均显著降低,GABA、SOD、GSH-Px水平均显著增高。亚低温银杏叶组与亚低温脑缺血组比较,Glu、GABA、SOD、GSH-Px、MDA水平均无显著性差异。结论脑缺血后,GBE清除氧自由基、降低"兴奋毒性"相关生化物质基础的作用受不同脑温的影响。亚低温状态下,GBE清除氧自由基、降低"兴奋毒性"相关生化物质基础的作用增强,从而增强GBE的神经保护作用。亚低温和GBE联合干预增强对缺血脑组织的保护作用,可能是亚低温作用为主,两种干预因素协同作用的结果。

Objective It is to explore the effect of Ginkgo biloba extract （GBE） on the concentration of Glu, GABA, SOD, GSH - Px and MDA in ischemic cerebral tissue under different cerebral temperature in rats. Methods The rat models of middle cerebral artery ischemia reperfusion were established and randomly divided into normal temperature sham operation group（group A）, normal temperature cerebral ischemia group （group B）, sub-hypothermia cerebral ischemia group （group C） , normal temperature GBE group（ group D） , mild high temperature GBE group （group E） , sub-hypothermia GBE group （group F） , all the groups were induced to target cerebral temperature, then the concentrations of Glu, GABA, SOD, GSH - Px and MDA in ischemic cerebral tissue in every group were determined. Results Compared with group A, the concentrations of Glu, GABA, and MDA were obviously increased, while the concentrations of SOD, GSH - P were significantly decreased in group B, group D and group E. Compared with group B, the concentrations of Glu and MDA were significantly decreased, while the concentrations of GABA, SOD and GSH - Px were significantly increased in group D, group group C, group F. Compared with group D, the concentrations of Glu and MDA were significantly increased, and the concentration of GABA, SOD and GSH -Px were significantly decreased in group E, but the concentration of Glu, MDA were significantly decreased and the concentration of GABA, SOD, GSH - Px were significantly increased in group C and group group F. There was no significant difference in the concentration of Glu, GABA, SOD, GSH -Px and MDA between group C and group F. Conclusion During the processes of cerebral ischemia, different brain temperature may affect the regulation on the biochemistry substance of GDE＇ s ＂cleaning oxygen free radical and decreasing exitotoxicity＂, then enhance the neuroprotective effect of GBE. it suggests that the enhanced neuroprotection in focal cerebral ischemia tissue of GBE group under subhypothermia isn＇t the result of either subhypothermia or GBE intervention factor, but the main effects of subhypothermia and cooperation of both.