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目的 探讨老龄大鼠全脑缺血再灌注损伤对颞叶、杏仁核和尾状核 N G F、 B D N F 的含量影响。方法 采用 Pulsinelli Brierley 4 血管阻塞法制作全脑缺血 15m in、再灌注 1h、6h、2d、4d、9d 模型,检测颞叶、杏仁核和尾状核 N G F、 B D N F 的表达。结果 全脑缺血再灌注损伤时,颞叶迅速出现中量 N G F 表达;杏仁核仅再灌注早期出现 N G F 表达量增加;尾状核 N G F 的表达很快消失。缺血再灌注损伤没有引起颞叶、杏仁核的 B D N F表达量改变;但引起尾状核 B D N F表达量增加。结论 颞叶具有较好的 N G F 保护机制,杏仁核对缺血再灌注损伤具有反应迅速、短期的 N G F 保护机制,而尾状核缺乏良好的 N G F 保护机制。颞叶和杏仁核具有良好的 B D N F 保护机制,尾状核具有反应迅速、作用持久的 B D N F保护机制。
Objective To investigate the effects of global cerebral ischemia-reperfusion injury on the contents of N G F and B D N F in temporal lobe, amygdala and caudate nucleus in aged rats. Methods Pulsinelli-Brierley 4 occlusion method was used to make models of global ischemia 15 mins, reperfusion 1h, 6h, 2d, 4d, 9d to detect the expressions of N G F and B D N F in temporal lobe, amygdala and caudate nucleus . Results During global cerebral ischemia-reperfusion, the expression of NGF in the temporal lobe rapidly appeared. The expression of NGF in the amygdala increased only in the early stage of reperfusion. The expression of NGF in the caudate nucleus quickly disappeared. Ischemia-reperfusion injury did not change the expression of B D N F in temporal lobe and amygdala, but increased the expression of B D N F in caudate nucleus. Conclusion The temporal lobe has a good mechanism of NGF protection. The amygdala has a rapid and short-term mechanism of NGF protection against ischemia-reperfusion injury, while the caudate nucleus lacks a good mechanism of NGF protection. Temporal lobe and amygdala have a good mechanism of B D N F protection, caudate nucleus has a rapid response, long lasting role of B D N F protection.