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目的观察大鼠脑缺血再灌注损伤基质金属蛋白酶(MMP-9)表达及神经调节素-1β(NRG-1β)的干预作用。方法取成年健康雄性Wister大鼠100只,应用线拴法经颈外-颈内动脉插线建立大脑中动脉闭塞再灌注(MCAO/R)动物模型,经颈内动脉单剂量注射1.5%NRG-1β5μL干预治疗。采用免疫组化、免疫荧光、免疫印迹法,观察脑组织MMP-9表达。结果脑缺血再灌注损伤可诱导脑组织MMP-9表达。随着缺血缺氧时间的延长,对照组MMP-9蛋白的表达逐渐增加,阳性细胞形态大小不一,分布于脑组织各区。NRG-1β治疗可降低MMP-9的表达水平,与对照组相应脑区相比,差异显著(P<0.01)。结论MMP-9参与脑缺血再灌注损伤后的炎症反应过程。NRG-1β可能通过调节脑组织中MMP-9的活性,干扰脑缺血再灌注损伤后炎症的发生发展过程,改善神经元的生存环境,延迟神经元损伤的时间和程度,进而对缺血性脑损伤具有积极的保护作用。
Objective To observe the effect of the expression of matrix metalloproteinase (MMP-9) and neuregulin-1β (NRG-1β) on focal cerebral ischemia-reperfusion injury in rats. Methods One hundred male Wister rats were randomly divided into two groups: MCAO / R model was established by cable-intercatenang-carotid artery intercalation and 1.5% NRG- 1β5μL intervention. Immunohistochemistry, immunofluorescence and Western blotting were used to observe the expression of MMP-9 in brain tissue. Results Cerebral ischemia-reperfusion injury can induce the expression of MMP-9 in brain tissue. With the prolongation of hypoxia / hypoxia time, the expression of MMP-9 in the control group gradually increased, the positive cells varied in size and distributed in various regions of brain tissue. NRG-1β treatment could reduce the expression of MMP-9, which was significantly different from the corresponding brain regions in the control group (P <0.01). Conclusion MMP-9 is involved in inflammatory reaction after cerebral ischemia-reperfusion injury. NRG-1β may interfere with the development of inflammation after cerebral ischemia-reperfusion injury by regulating the activity of MMP-9 in brain tissue, improve the living environment of neurons, delay the time and extent of neuronal damage, Brain damage has a positive protective effect.