title: Autophagy suppression by exercise pretreatment and p38 inhibition is neuroprotective in cerebral ischemia.
abstract: 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.
authors.affiliation: Department of Rehabilitation, Huashan Hospital, Fudan University, Shanghai 200040, China.
authors.forename: Li
authors.initials: L
authors.lastname: Zhang
authors.affiliation: Department of Rehabilitation, Huashan Hospital, Fudan University, Shanghai 200040, China.
authors.forename: Wenxiu
authors.initials: W
authors.lastname: Niu
authors.affiliation: Department of Rehabilitation, Huashan Hospital, Fudan University, Shanghai 200040, China.
authors.forename: Zhijie
authors.initials: Z
authors.lastname: He
authors.affiliation: Department of Rehabilitation, Huashan Hospital, Fudan University, Shanghai 200040, China.
authors.forename: Qi
authors.initials: Q
authors.lastname: Zhang
authors.affiliation: Department of Rehabilitation, Huashan Hospital, Fudan University, Shanghai 200040, China; State Key Laboratory of Medical Neurobiology, Fudan University, Shanghai 200032, China.
authors.forename: Yi
authors.initials: Y
authors.lastname: Wu
authors.affiliation: Department of Rehabilitation, Huashan Hospital, Fudan University, Shanghai 200040, China.
authors.forename: Congyu
authors.initials: C
authors.lastname: Jiang
authors.affiliation: Department of Rehabilitation, Huashan Hospital, Fudan University, Shanghai 200040, China.
authors.forename: Chaozheng
authors.initials: C
authors.lastname: Tang
authors.affiliation: Department of Rehabilitation, Huashan Hospital, Fudan University, Shanghai 200040, China; State Key Laboratory of Medical Neurobiology, Fudan University, Shanghai 200032, China.
authors.forename: Yongshan
authors.initials: Y
authors.lastname: Hu
authors.affiliation: Department of Rehabilitation, Huashan Hospital, Fudan University, Shanghai 200040, China. Electronic address: shannonjj@126.com.
authors.forename: Jie
authors.initials: J
authors.lastname: Jia
mesh_terms: D000818:Animals; D051017:Apoptosis Regulatory Proteins; D001343:Autophagy / Q000502:physiology*; D002545:Brain Ischemia / Q000378:metabolism / Q000473:pathology*; D006360:Heat-Shock Proteins / Q000378:metabolism; D020244:Infarction, Middle Cerebral Artery / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D002546:Ischemic Attack, Transient / Q000201:enzymology / Q000235:genetics / Q000473:pathology; D020935:MAP Kinase Signaling System / Q000502:physiology*; D008297:Male; D009419:Nerve Tissue Proteins / Q000037:antagonists & inhibitors* / Q000502:physiology; D009474:Neurons / Q000201:enzymology / Q000473:pathology; D010766:Phosphorylation; D010805:Physical Conditioning, Animal / Q000502:physiology*; D011499:Protein Processing, Post-Translational; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000517:prevention & control*; D012420:Running; D000071456:Sequestosome-1 Protein; D048051:p38 Mitogen-Activated Protein Kinases / Q000037:antagonists & inhibitors* / Q000502:physiology
chemical_list: D051017:Apoptosis Regulatory Proteins; D006360:Heat-Shock Proteins; D009419:Nerve Tissue Proteins; D000071456:Sequestosome-1 Protein; C491079:Sqstm1 protein, rat; D048051:p38 Mitogen-Activated Protein Kinases
keywords: Autophagy; Cerebral ischemia; Exercise pretreatment; Neuroprotection; p38