Journal
BRAIN RESEARCH
Volume 1587, Issue -, Pages 127-132Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.brainres.2014.08.067
Keywords
Autophagy; Cerebral ischemia; Neuroprotection; Exercise pretreatment; p38
Categories
Funding
- Chinese National Nature Science Foundation [81472151, 81472150, 81171855, 81171856, 81272169, 81201502]
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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.
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