论文部分内容阅读
目的研究局灶性脑缺血再灌注损伤中iNOS在不同脑区的表达。方法用改良的血管内栓线技术制造大鼠局灶性脑缺血与再灌注模型,应用免疫组织化学技术检测脑组织中的iNOS的表达。结果(1)脑缺血再灌注损伤24h后,缺血组缺血侧大脑皮层、海马CA1区、CA3区神经元iNOS的表达显著增强,与正常对照组比较有显著性差异(P<0·05);(2)脑缺血再灌注损伤24h后,缺血组对照侧大脑皮层、海马CA1区、CA3区神经元iNOS的表达也明显增强,与正常对照组比较有显著性差异(P<0·05);(3)与对照侧比较,脑缺血再灌注大鼠缺血侧皮质的iNOS表达显著增强(P<0·05),而海马CA1区、CA3区缺血侧的iNOS表达与对照侧相比无显著性差异(P>0·05)。结论局灶性脑缺血再灌注损伤后,缺血侧皮层和海马iNOS表达显著升高,未缺血脑区(对照侧)iNOS反应性也较对照组者升高。
Objective To study the expression of iNOS in different brain regions during focal cerebral ischemia-reperfusion injury. Methods The model of focal cerebral ischemia and reperfusion was established by modified intravascular plug technique. The expression of iNOS in brain tissue was detected by immunohistochemistry. Results (1) The expression of iNOS in the ischemic cortex, hippocampal CA1 and CA3 neurons was significantly increased at 24 h after cerebral ischemia / reperfusion injury in ischemic rats, which was significantly different from the normal control group (P <0. 0.05). (2) After 24h of cerebral ischemia-reperfusion injury, the expression of iNOS in cerebral cortex, hippocampal CA1 and CA3 area in ischemic group was significantly increased compared with that in normal control group (P < 0.05). (3) Compared with the control group, the iNOS expression of ischemic cortex in cerebral ischemia-reperfusion rats was significantly increased (P <0.05), while the expression of iNOS in hippocampal CA1 and CA3 regions There was no significant difference between the control group and the control group (P> 0.05). Conclusions The expression of iNOS in the ischemic cortex and hippocampus is significantly increased after focal cerebral ischemia-reperfusion injury, and the iNOS reactivity in the non-ischemic brain area (control side) is also higher than that in the control group.