Autophagy suppression by exercise pretreatment and p38 inhibition is neuroprotective in cerebral ischemia

被引：27

作者：

Zhang, Li ^{[1
]}

Niu, Wenxiu ^{[1
]}

He, Zhijie ^{[1
]}

Zhang, Qi ^{[1
]}

Wu, Yi ^{[1
,2
]}

Jiang, Congyu ^{[1
]}

Tang, Chaozheng ^{[1
]}

Hu, Yongshan ^{[1
,2
]}

Jia, Jie ^{[1
]}

机构：

[1] Fudan Univ, Huashan Hosp, Dept Rehabil, Shanghai 200040, Peoples R China

[2] Fudan Univ, State Key Lab Med Neurobiol, Shanghai 200040, Peoples R China

来源：

BRAIN RESEARCH | 2014年 / 1587卷

关键词：

Autophagy; Cerebral ischemia; Neuroprotection; Exercise pretreatment; p38; ACTIVATED PROTEIN-KINASE; BRAIN-INJURY; CELL-DEATH; ARTERY OCCLUSION; NEURONAL AUTOPHAGY; PHYSICAL-ACTIVITY; GROWTH-FACTOR; RAT MODEL; STROKE; REPERFUSION;

D O I：

10.1016/j.brainres.2014.08.067

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Autophagy is a degradative mechanism for cellular proteins and organelles, but its role in the nervous system is still not clear. In the present study, we found that exercise pretreatment and p38 inhibition had influence on autophagic process after cerebral ischemia, contributing to their neuroprotective effects. We examined the levels of p62 and phosphorylated ERK1/2 as an autophagic marker and cell-survival marker respectively after cerebral ischemic injury. The brain infarction volume after ischemia was measured as well. Both treadmill training pretreatment and p38 inhibition decreased the degradation of p62, promoted the phosphorylation of ERK1/2, and alleviated the brain infarction, indicating that these treatments could provide neuroprotection in cerebral ischemic injury via autophagy suppression. (C) 2014 Elsevier B.V. All rights reserved.

引用

页码：127 / 132

页数：6

共 55 条

[1] Neuroprotection associated with running: Is it a result of increased endogenous neurotrophic factors?
Ang, ET
Wong, PTH
Moochhala, S
Ng, YK
[J]. NEUROSCIENCE, 2003, 118 (02) : 335 - 345
[2] Barone FC, 2001, J PHARMACOL EXP THER, V296, P312
[3] Rapamycin protects against middle cerebral artery occlusion induced focal cerebral ischemia in rats
Chauhan, Anjali
Sharma, Uma
Jagannathan, N. R.
Reeta, K. H.
Gupta, Yogendra Kumar
[J]. BEHAVIOURAL BRAIN RESEARCH, 2011, 225 (02) : 603 - 609
[4] Eaten alive - Autophagy and neuronal cell death after hypoxia-ischemia
Chu, Charleen T.
[J]. AMERICAN JOURNAL OF PATHOLOGY, 2008, 172 (02) : 284 - 287
[5] PROPOFOL PREVENTS CEREBRAL ISCHEMIA-TRIGGERED AUTOPHAGY ACTIVATION AND CELL DEATH IN THE RAT HIPPOCAMPUS THROUGH THE NF-κB/P53 SIGNALING PATHWAY
Cui, D. R.
Wang, L.
Jiang, W.
Qi, A. H.
Zhou, Q. H.
Zhang, X. L.
[J]. NEUROSCIENCE, 2013, 246 : 117 - 132
[6] Constraint-induced movement therapy and rehabilitation exercises lessen motor deficits and volume of brain injury after striatal hemorrhagic stroke in rats
DeBow, SB
Davies, MLA
Clarke, HL
Colbourne, F
[J]. STROKE, 2003, 34 (04) : 1021 - 1026
[7] Exercise preconditioning ameliorates inflammatory injury in ischemic rats during reperfusion
Ding, YH
Young, CN
Luan, XD
Li, J
Rafols, JA
Clark, JC
McAllister, JP
Ding, YC
[J]. ACTA NEUROPATHOLOGICA, 2005, 109 (03) : 237 - 246
[8] Guidelines for the Prevention of Stroke in Patients With Stroke or Transient Ischemic Attack A Guideline for Healthcare Professionals From the American Heart Association/American Stroke Association
Furie, Karen L.
Kasner, Scott E.
Adams, Robert J.
Albers, Gregory W.
Bush, Ruth L.
Fagan, Susan C.
Halperin, Jonathan L.
Johnston, S. Claiborne
Katzan, Irene
Kernan, Walter N.
Mitchell, Pamela H.
Ovbiagele, Bruce
Palesch, Yuko Y.
Sacco, Ralph L.
Schwamm, Lee H.
Wassertheil-Smoller, Sylvia
Turan, Tanya N.
Wentworth, Deidre
[J]. STROKE, 2011, 42 (01) : 227 - 276
[9] Gabryel B, 2012, PHARMACOL REP, V64, P1
[10] Enhancement of Autophagic Flux after Neonatal Cerebral Hypoxia-Ischemia and Its Region-Specific Relationship to Apoptotic Mechanisms
Ginet, Vanessa
Puyal, Julien
Clarke, Peter G. H.
Truttmann, Anita C.
[J]. AMERICAN JOURNAL OF PATHOLOGY, 2009, 175 (05) : 1962 - 1974

← 1 2 3 4 5 6 →