摘要
目的观察大鼠局灶性脑缺血再灌注损伤(CIRI)后杏仁核基质金属蛋白酶-9(MMP-9)、水通道蛋白4(AQP4)、热休克蛋白70(HSP70)的表达变化,检测脑水肿,探讨其可能机制。方法线栓法制备大鼠大脑中动脉闭塞2h/再灌注24h模型。AutoCAD软件计算缺血侧脑水肿程度;免疫组织化学法检测杏仁核MMP-9、AQP4以及HSP70表达,计数阳性细胞数,图像分析系统作半定量分析。结果局灶性脑缺血2h/再灌注24h后,大鼠杏仁核MMP-9、AQP4及HSP70阳性细胞计数显著增多[MMP-9(38.70±1.51)vs(4.00±1.27),AQP4(28.35±2.00)vs(1.00±0.80),HSP70(21.58±1.75)vs(2.00±0.99),(P<0.01)],脑水肿程度[模型组(30.25±9.20)%,假手术组0,(P<0.01)]。结论CIRI后杏仁核MMP-9、AQP4表达增加,参与继发性血脑屏障的开放和脑水肿的发生;而杏仁核HSP70表达增加,提示CIRI后杏仁核呈现明显的缺血性损伤反应。
Objective To observe the changes of the expression of matrix metalloproteinases （MMP9）, aquaporins（AQP4） and heat shock protein（HSP70） after focal cerebral ischemia-reperfusion injury（CIRI） in amygdala of rats, to detect the degree of cerebral edema and to discuss the possible mechanism. Methods The right middle cerebral artery in rats were occluded by inserting a thread through internal carotid artery for 2 h, and then reperfused for 24 h. The Auto CAD image analytic software calculates degree of the cerebral edema. The expression of MMP-9, AQP4 and HSP70 protein were examined by immunohistochemistry in the amygdala, and the positive staining cells were calculated with image analysis system in semi-quantitative analysis. Results Compared with sham group, MMP-9, AQP4 and HSP70 positive staining cell in model group obviously increased, MMP-9（38. 70±1. 51） vs （4.00±1.27）, （P〈0.01） ; AQP4（28. 35±2. 00） vs （1.00±0.80）, （P〈0.01）; HSP70（21. 58±1. 75） vs （2.00±0.99）, （P（0.01）. Cerebral edema was （30. 25±9. 20）;in model group vs sham group 0（P（0.01）. Conclusion CIRI could increase the expression of MMP-9, AQP4 and HSP70 in amygdala. High expression of MMP-9 and AQP4 in amygdala may involve in secondary cerebral edema, the increase of HSP70 showed an evident ischemic injury response in amygdala after CIRI.
出处
《福建医科大学学报》
2007年第3期203-206,共4页
Journal of Fujian Medical University
基金
福建省自然科学基金资助项目(C0110010)
