brain research 1605 (2015) 1–11
Available online at
ate/brainres
Research Report
Inhibition of adenosine monophosphate-activated
protein kinase reduces glial cell-mediated
inflammation and induces the expression of Cx43
in astroglias after cerebral ischemia
Yu Ma a,b, Juan Bub, Hui Dangb, Jing Shab, Yan Jingb, AI Shan-jiangb,
n
Hongyan Lib, Yi Zhua,b,
aXinjiang Clinical Medical College, Anhui Medical University, Hefei, China
bDepartment of Neurology, Xinjiang Uygur Autonomous Region People’s Hospital, Urumqi, China
article info abstract
Article history: We investigated the protective effect of adenosine monophosphate-activated protein kinase
Accepted 13 November 2014 (AMPK) inhibition on cerebral ischemic injury of mice, and characterized the role of AMPK
Available online 22 January 2015 inhibition on astrocytes, microglias, and neuroinflammation. Focal cerebral ischemia was
Keywords: induced by middle cerebral artery occlusion (MCAO) in male Kunming mice, pound C
Cerebral ischemia-reperfusion was used to inhibit AMPK activity. The neurobehavioral scores, infarct volumes, phosphoryla-
fl
injury tion of AMPK, activation of the glial cells, levels of connexin 43 (Cx43), and related in ammatory
AMPK
Cx43 activated after cerebral ischemia. AMPK inhibition reduced infarct size and improved neuro-
Astrocyte logical es after 24 h reperfusion of mice. Furthermore, our study revealed that the
Microglia mechanisms of neuroprotection of AMPK inhibition may be as follows: (1) inhibiting the
Neuroinflammation excessive activation of astrocyte and microglia cells, (2) stabilizing the expression of protective
proteins such as Cx43 in astroglias, and (3) inhibiting the release of microglial pro-inflammatory
factors. These results demonstrated that AMPK inhibition attenuated cerebral ischemic injury,
at least in part, by glial cell-mediated protective effects in mice.
& 2015 Elsevier . All rights reserved.
1. Introduction oxidative
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