The role of autophagic and lysosomal pathways in ischemic brain injury

查看全文 作　　者：Zhaohua [1]Gu;Yinyi [2]Sun;Kangyong [1,2]Liu;Fen [3]Wang;Ting [2]Zhang;Qiang [2]Li;Liwei [4]Shen;Ling [4]Zhou;Liang [1]Dong;Nan [1]Shi;Qian [1]Zhang;Wei [1]Zhang;Meizhen [1]Zhao;Xiaojiang [2]Sun

机构地区：[1]Department of Neurology, Shanghai Pudong New Area Zhoupu Hospital;[2]Department of Neurology, the Sixth People's Hospital of Shanghai, Shanghai Jiao Tong University;[3]Department of Neurobiology, Suzhou University School of Medicine;[4]Department of Neurology, the Fifth People's Hospital of Shanghai, Fudan University

出　　处：《Neural Regeneration Research》索引2013年第8卷第23期,共9页

基　　金：supported by grants from the National Natural Science Foundation of China,No.31171014 and No.30970869;the Project of Science and Technology Commission of ShanghaiCity,No.09DZ1950400;Board of Health of Shanghai,China,No.2008086;the Youth Projects of National Natural Science Foundation of China,No.31100783;Youth Key Project in Shanghai College of Medicine of Fudan University,No.09-L37 摘　　要：Autophagy is involved in neural cell death after cerebral ischemia. Our previous studies showed that rapamycin-induced autophagy decreased the rate of apoptosis, but the rate of apoptosis was in-creased after the autophagy inhibitor, 3-methyladenine, was used. In this study, a suture-occluded method was performed to generate a rat model of brain ischemia. Under a transmission electron microscope, autophagic bodies and autophagy lysosomes were markedly accumulated in neurons at 4 hours post brain ischemic injury, with their numbers gradually reducing over time. Western blotting demonstrated that protein levels of light chain 3-II and cathepsin B were significantly in-creased within 4 hours of ischemic injury, but these levels were not persistently upregulated over time. Confocal microscopy showed that autophagy was mainly found in neurons with positive light chain 3 signal. Injection of rapamycin via tail vein promoted the occurrence of autophagy in rat brain tissue after cerebral ischemia and elevated light chain 3 and cathepsin B expression. However, in-jection of 3-methyladenine significantly diminished light chain 3-II and cathepsin B expression. Results verified that autophagic and lysosomal activity is increased in ischemic neurons. Abnormal components in cells can be eliminated through upregulating cell autophagy or inhibiting autophagy after ischemic brain injury, resulting in a dynamic balance of substances in cells. Moreover, drugs that interfere with autophagy may be potential therapies for the treatment of brain injury. 关键词：缺血性脑损伤溶酶体自噬神经细胞死亡组织蛋白酶B WESTERN印迹透射电子显微镜共聚焦显微镜

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The role of autophagic and lysosomal pathways in ischemic brain injury

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