Details

Autor(en) / Beteiligte

• Gu, Zhaohua
• Sun, Yinyi
• Liu, Kangyong
• Wang, Fen
• Zhang, Ting
• Li, Qiang
• Shen, Liwei
• Zhou, Ling
• Dong, Liang
• Shi, Nan
• Zhang, Qian
• Zhang, Wei
• Zhao, Meizhen
• Sun, Xiaojiang

Titel

The role of autophagic and lysosomal pathways in ischemic brain injury

Ist Teil von

• Neural regeneration research, 2013-08, Vol.8 (23), p.2117-2125

Ort / Verlag

India: Medknow Publications and Media Pvt. Ltd

Erscheinungsjahr

2013

Quelle

EZB Electronic Journals Library

Beschreibungen/Notizen

• 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 3-11 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 3-11 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.