外周静脉给予PACAP38对脑缺血再灌注损伤的保护作用  

The Protective effect of PACAP38 through peripheral vein in rats after cerebral ischemia-reperfusion injury

作　　者：史秀丽[1] 王传明[1] 杨莹[1] 傅佳[1] 

机构地区：[1]安徽医科大学第一附属医院神经内科,合肥230022

出　　处：《安徽医学》2009年第5期499-501,共3页Anhui Medical Journal

基　　金：安徽省教育厅自然科学研究基金资助项目(2005KJ250)

摘　　要：目的探讨通过外周静脉途径给予垂体腺苷酸环化酶激活肽38(PACAP38)对大鼠局灶性脑缺血再灌注损伤的保护作用。方法线栓法制作大鼠大脑中动脉梗阻模型,脑缺血2h再灌注后6h、12h、24h、48h、72h时分别外周静脉途径给予PACAP38,维持48h后取出脑组织,测定脑梗死体积、超氧化物歧化酶(SOD)活性、丙二醛(MDA)和一氧化氮(NO)含量,并设立对照组,对照组静脉输入生理盐水。结果PACAP38能显著减轻脑梗死体积,增加SOD活性,降低MDA和NO含量,再灌注后6h时给予PACAP38上述改变最为明显。结论PACAP38能有效经外周静脉途径通过血脑屏障,发挥减轻局灶性脑缺血再灌注损伤的作用,其机制与减少自由基生成有关。Objective To investigate the protective effect of given PACAP38 through peripheral vein in rats after focal cerebral ischemia - reperfusion injury. Methods The models of middle cerebral artery occlusion in rats were established with suture - occluded method. PACAP38 was injected at 6h, 12h, 24h, 48h and 72h respectively after 2h - cerebral ischemia through peripheral vein. which was 48h, focal cerebral isehemia reperfusion. Then picked up the Brain tissues were removed after PACAP38 being maintained 48 hours, and the area of cerebral infarction were measured, the activity of superoxide dismutase （ SOD）, the content of malondialdehyde （MDA） and nitric oxide （NO） were detected. The control group which was injected normal saline （NS） were established as well. Results PACAP38 could reduce the area of cerebral infarction significantly, increase the activity of SOD and decrease the content of MDA and NO. The above items were changed obviously at 6h after cerebral reperfusion. Conclusion PACAP38 given through peripheral vein effectively could penetrate the blood - brain - barrier and lighten the ischemia - reperfusion injury of focal cerebral. The mechanism of it was related to reducing the generation of free radicals.

关 键 词：垂体腺苷酸环化酶激活肽 局灶性脑缺血再灌注损伤 神经保护 

分 类 号：R743[医药卫生—神经病学与精神病学]