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阿司匹林预处理对大鼠脑缺血再灌注损伤的神经保护作用
Neuroprotective mechanism of aspirin preconditioning in cerebral ischemia reperfusion injury on Sprague-Dawley rats
【摘要】 目的:观察阿司匹林(ASA)预处理对大鼠局灶性脑缺血再灌注损伤(I/R)的神经保护作用,并对其作用机制进行探讨。方法:复制大鼠大脑中动脉缺血再灌注模型,分别采用TTC染色法、神经功能缺损评分法观察ASA预处理对大鼠脑梗死体积和神经功能评分的影响,以及对脑组织中超氧化物歧化酶(SOD)、丙二醛(MDA)和血前列环素I2(PGI2)/血栓素A2(TXA2)的影响。结果:ASA能够降低I/R大鼠脑梗死体积和神经功能评分,增加脑组织中SOD的活性,降低MDA的含量,升高血PGI/TXA2的比值。结论:ASA对大鼠脑缺血再灌注损伤有一定保护作用,其作用机制与增加脑组织中SOD的活性、降低MDA的含量、提高血PGI2/TXA2的比值有关。
【Abstract】 Objective:To observe neuroprotective mechanism of aspirin preconditioning in cerebral ischemia reperfusion injury on Sprague-Dawley rats.Methods:Adult male SD rats were subjected to MCAO/reperfusion(MCAO/R).The neurological scores were made on Zealonga 5-point scale.The volume of infarction was measured by TTC staining.Superoxide dismutase(SOD),malondialdehyde(MDA),prostacyclin(PGL2)and thromboxane(TXA2) were determined by commercial kits reagent.Results:Aspirin preconditioning decreased infatct volume,protected neurons and improved behavioral outcomes in MCAO/R rats.Aspirin preconditioning also significantly reduced MDA content,increased SOD activities and PGI/TXA2.Conclusion:Aspirin preconditioning has neuroprotective mechanism in cerebral ischemia reperfusion injury.Its mechanism may be the inhibition of SOD activity,the rise of PGI2/TXA2 and the reduction of MDA content.
【Key words】 aspirin; preconditioning; cerebral ischemia reperfusion injury; superoxide dismutase; malondialdehyde; prostacyclin/thromboxane;
- 【文献出处】 临床医药实践杂志 ,Proceeding of Clinical Medicine , 编辑部邮箱 ,2007年11期
- 【分类号】R96
- 【被引频次】1
- 【下载频次】104