自噬在大鼠脑缺血再灌注损伤中的作用及机制研究  

Study on the role and mechanism of autophagy in cerebral ischemia-reperfusion injury in rats

作　　者：陈运转 吕爱红 王军杰 辛凯[2] 赵曼[1] CHEN Yunzhuan;LYU Aihong;WANG Junjie;XIN Kai;ZHAO Man(Zhengzhou People's Hospital,Zhengzhou 450000,China;The Third Affiliated Hospital of Henan University of Traditional Chinese Medicine,Zhengzhou 450000,China)

机构地区：[1]郑州人民医院,河南郑州450000 [2]河南中医药大学第三附属医院,河南郑州450000

出　　处：《中国实用神经疾病杂志》2020年第24期2117-2122,共6页Chinese Journal of Practical Nervous Diseases

基　　金：河南省中医药科学研究专项课题(编号:2018ZY2057)。

摘　　要：目的通过构建大鼠缺血再灌注损伤模型,观察再灌注后自噬现象的发生,探讨自噬在脑缺血再灌注损伤中的作用。方法选用健康Sprague-Dawley(SD)大鼠(n=108),随机分为3组各36只(1)假手术组;(2)对照组;(3)三-甲基腺嘌呤(3-MA)组,然后根据再灌注时间(6 h、12 h和24 h)将各组随机分为3个亚组各12只。根据神经行为学评分、TTC染色、脑组织含水量、透射电子显微镜几方面结果进行统计学分析。结果假手术组无症状,TTC染色未见梗死灶,脑组织含水量最少,电镜下海马神经细胞细胞器正常,无自噬现象。对照组症状较3-MA组减轻(P<0.05),梗死灶占比较3-MA组降低(P<0.05),脑组织含水量较3-MA组减少(P<0.05),细胞器破坏较3-MA组减轻,自噬溶酶体较3-MA组增多。结论缺血再灌注可致神经细胞损伤,细胞出现自噬现象,表现为大鼠神经功能缺失,缺血侧脑组织见梗死灶,梗死灶内海马神经细胞受损,细胞内自噬溶酶体显著增多。在脑缺血再灌注损伤中,抑制细胞自噬可致神经元损伤加重,自噬的激活可能对神经细胞发挥保护作用。Objective To establish the model of ischemia-reperfusion injury in rats,observe the occurrence of autophagy after reperfusion,explore the mechanism of autophagy in cerebral ischemia-reperfusion injury,and may be an important pathogenesis of lupus encephalopathy.To provide a clinical basis for regulating autophagy as a theoretical basis for lupus encephalopathy.Methods Healthy Sprague-Dawley(SD)rats(n=108)were randomly divided into 3 groups①sham operation group;②control group;③tri-methyladenine(3-MA)group,and then according to the perfusion time(6h,12h and 24h)divided each group into 3 subgroups at random.Statistical analysis was performed based on the results of neurobehavioral scoring,TTC staining,water content of brain tissue,transmission electron microscope.Results The sham operation group was asymptomatic,no infarcts were observed by TTC staining,the brain tissue had the least water content,the hippocampal nerve cell organelles were normal under electron microscope,and there was no autophagy.The symptoms in the control group were alleviated compared with the 3-MA group(P<0.05).The percentage was lower than that of 3-MA group(P<0.05),the water content of brain tissue was lower than that of 3-MA group(P<0.05),the destruction of organelles was less than that of 3-MA group,and the autophagolysosome was more than that of 3-MA group.Conclusion Microangiopathy and thrombosis are the main pathological basis of lupus encephalopathy,and autophagy disorder is shown to be related to the pathogenesis of systemic lupus erythematosus.Ischemia-reperfusion can cause nerve cell damage,autophagy occurs in the cells,which is manifested by the loss of nerve function in rats,infarct focus is seen in ischemic lateral brain tissue,hippocampal nerve cells in the infarct focus are damaged,and intracellular autolysosome is significant Increased,in cerebral ischemia-reperfusion injury,3-MA as an inhibitor of autophagy can aggravate neuronal damage,activation of autophagy may play a neuroprotective role,and resetting autophagy flux

关 键 词：自噬 缺血再灌注 3-甲基腺嘌呤 神经细胞 SPRAGUE-DAWLEY大鼠 

分 类 号：R-332[医药卫生]