title: Hypoxia induces microglia autophagy and neural inflammation injury in focal cerebral ischemia model.
abstract: Much evidence demonstrated that autophagy played an important role in neural inflammation response after ischemia stroke. However, the specific effect of microglia autophagy in cerebral ischemia is still unknown. In the current study, we constructed focal cerebral ischemia model by permanent middle cerebral artery occlusion (pMCAO) in mice. We detected microglia autophagy and inflammation response in vivo, and observed infarct brain areas, edema formation, and neurological deficits of mice. We found that pMCAO induced microglia autophagy and inflammatory response. The suppression of autophagy using either pharmacologic inhibitor (3-MA) not only decreased the microglia autophagy and inflammatory response, but also significantly decreased infarct size, edema formation and neurological deficits in vivo. Taken together, these results suggested that cerebral ischemia induced microglia autophagy contributed to ischemic neural inflammation and injury. In addition, our findings also provided novel therapeutic strategy for ischemic stroke.
authors: Department of Neurology, Yongchuan Hospital, Chongqing Medical University, Chongqing 402160, China.
authors: Zhao
authors: Z
authors: Yang
authors: Department of Neurology, Yongchuan Hospital, Chongqing Medical University, Chongqing 402160, China.
authors: Lina
authors: L
authors: Zhong
authors: Department of Neurology, Yongchuan Hospital, Chongqing Medical University, Chongqing 402160, China.
authors: Shanchuan
authors: S
authors: Zhong
authors: Department of Neurosurgery, The 476th Hospital of PLA, Fuzhou, Fujian 350025, China.
authors: Ronghua
authors: R
authors: Xian
authors: Department of Neurosurgery, The 476th Hospital of PLA, Fuzhou, Fujian 350025, China. Electronic address: ytt83812280@sina.com.
authors: Bangqing
authors: B
authors: Yuan
mesh_terms: D000225:Adenine / Q000031:analogs & derivatives / Q000494:pharmacology; D000818:Animals; D001343:Autophagy / Q000187:drug effects*; D001921:Brain / Q000098:blood supply; D015687:Cell Hypoxia; D002536:Cerebral Arteries; D004195:Disease Models, Animal; D020244:Infarction, Middle Cerebral Artery / Q000188:drug therapy* / Q000473:pathology*; D007249:Inflammation / Q000473:pathology; D053583:Interleukin-1beta / Q000096:biosynthesis; D015850:Interleukin-6 / Q000096:biosynthesis; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D017628:Microglia / Q000166:cytology / Q000473:pathology; D020123:Sirolimus / Q000494:pharmacology; D020521:Stroke / Q000188:drug therapy* / Q000473:pathology*; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis
chemical_list: C587672:IL1B protein, mouse; D053583:Interleukin-1beta; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha; C025946:3-methyladenine; D000225:Adenine; D020123:Sirolimus
keywords: Autophagy; Hypoxia; Ischemia; Microglia