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目的:采用免疫组化技术,研究全脑缺血后再灌不同时点大鼠皮层神经元AMPA受体亚单位GluR2表达的变化,探讨GluR2在缺血性神经元损伤中的作用。方法:将36只SD大鼠随机分为6组,即正常组、缺血再灌注后2h、12h、24h、48h、72h 5个时间点组。参照改良的Pulsinelli四血管闭塞法制备全脑缺血大鼠模型,缺血再灌后的大鼠分别在存活2h、12h、24h、48h及72h后采用免疫组化法测定皮层神经元GluR2的表达量。结果:模型再灌5个时点之间SD大鼠皮层神经元GluR2表达量没有统计学差异(P>0.05),但与正常组相比,各组的的表达量明显降低(P<0.05)。结论:脑缺血再灌后皮层神经元AMPA受体亚单位GluR2表达减少,介导胞外Ca2+内流,引起神经细胞死亡。
OBJECTIVE: To study the effect of GluR2 on ischemic neuronal damage by immunohistochemistry in order to study the changes of GluR2 expression in AMPA receptor subunit of rat cortical neurons at different time points after global cerebral ischemia / reperfusion. Methods: Thirty-six Sprague-Dawley rats were randomly divided into 6 groups: normal group, 2h, 12h, 24h, 48h, 72h after ischemia-reperfusion. The rat models of global cerebral ischemia were established according to the modified Pulsinelli four-vessel occlusion method. The expression of GluR2 in cortical neurons was determined by immunohistochemistry after 2 h, 12 h, 24 h, 48 h and 72 h after ischemia / reperfusion the amount. Results: There was no significant difference in GluR2 expression in SD rat cortical neurons at 5 time point after reperfusion (P> 0.05), but the expression of GluR2 in each group was significantly lower than that in normal group (P <0.05) . CONCLUSION: After cerebral ischemia and reperfusion, the expression of GluR2, a subunit of AMPA receptor in cortical neurons, is decreased, which mediates the influx of extracellular Ca2 +, resulting in the death of nerve cells.