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目的研究Apelin-13侧脑室注射对大鼠脑缺血再灌注损伤的保护作用及相关机制。方法侧脑室埋管后,采用线栓法制备大鼠大脑中动脉栓塞模型,脑缺血2 h后侧脑室注射给药。再灌注24 h后进行Zea-Longa神经功能评分;TTC染色法测定大鼠脑梗死面积;试剂盒测定大鼠脑组织内诱导型一氧化氮合酶(inducible nitric oxide synthase,i NOS)和谷胱甘肽过氧化物酶(glutathione peroxidase,GSH-PX)的活性;Western blot法测大鼠脑组织Bcl-2、Bax和Caspase-3三种蛋白的表达水平。结果 Apelin-13(1.0μg·kg-1)侧脑室给药能改善大脑的神经功能,减少脑缺血面积,降低i NOS活性,增加GSH-PX活性,增加Bcl-2的表达,减少Bax和Caspase-3的表达。结论Apelin-13对缺血再灌注脑组织保护的可能机制包括降低NO水平,加强自由基清除,以及调节凋亡相关蛋白表达。
Objective To study the protective effect of Apelin-13 intracerebroventricular injection on cerebral ischemia-reperfusion injury in rats and its related mechanisms. Methods After intracerebroventricular catheterization, the middle cerebral artery occlusion model was established by thread occlusion. The intracerebroventricular injection was given 2 h after cerebral ischemia. The neurological score of Zea-Longa was evaluated 24 h after reperfusion. The area of cerebral infarction was determined by TTC staining. The expression of inducible nitric oxide synthase (iNOS) and glutathione The activity of glutathione peroxidase (GSH-PX) was detected by Western blot. The expression of Bcl-2, Bax and Caspase-3 in brain tissue of rats were detected by Western blot. Results Intracerebroventricular administration of Apelin-13 (1.0μg · kg -1) could improve the neurological function, reduce the area of cerebral ischemia, decrease the activity of iNOS, increase the activity of GSH-PX, increase the expression of Bcl-2, Caspase-3 expression. Conclusion The possible mechanisms by which Apelin-13 protects brain tissue from ischemia-reperfusion include decreasing NO level, enhancing free radical scavenging, and regulating apoptosis-related protein expression.