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Glutathione suppresses cerebral infarct volume and cell death after ischemic injury: involvement of FOXO3 inactivation and Bcl2 expression

Authors
 Juhyun Song  ;  Joohyun Park  ;  Yumi Oh  ;  Jong Eun Lee 
Citation
 OXIDATIVE MEDICINE AND CELLULAR LONGEVITY, Vol.2015 : 426069, 2015 
Journal Title
 OXIDATIVE MEDICINE AND CELLULAR LONGEVITY 
ISSN
 1942-0900 
Issue Date
2015
MeSH
Animals ; Antioxidants/pharmacology ; Antioxidants/therapeutic use ; Blood-Brain Barrier/metabolism ; Brain/metabolism ; Brain/pathology ; Brain Ischemia/drug therapy* ; Brain Ischemia/metabolism ; Brain Ischemia/pathology ; Cell Death/drug effects ; Cell Hypoxia ; Cell Line ; Forkhead Box Protein O3 ; Forkhead Transcription Factors/metabolism* ; Gene Expression Regulation* ; Glutathione/pharmacology ; Glutathione/therapeutic use* ; Male ; Mice ; Oxidative Stress/drug effects ; Phosphatidylinositol 3-Kinases/metabolism ; Proto-Oncogene Proteins c-bcl-2/genetics* ; Proto-Oncogene Proteins c-bcl-2/metabolism* ; Rats ; Rats, Sprague-Dawley ; Reactive Oxygen Species/metabolism ; Signal Transduction/drug effects
Abstract
Ischemic stroke interrupts the flow of blood to the brain and subsequently results in cerebral infarction and neuronal cell death, leading to severe pathophysiology. Glutathione (GSH) is an antioxidant with cellular protective functions, including reactive oxygen species (ROS) scavenging in the brain. In addition, GSH is involved in various cellular survival pathways in response to oxidative stress. In the present study, we examined whether GSH reduces cerebral infarct size after middle cerebral artery occlusion in vivo and the signaling mechanisms involved in the promotion of cell survival after GSH treatment under ischemia/reperfusion conditions in vitro. To determine whether GSH reduces the extent of cerebral infarction, cell death after ischemia, and reperfusion injury, we measured infarct size in ischemic brain tissue and the expression of claudin-5 associated with brain infarct formation. We also examined activation of the PI3K/Akt pathway, inactivation of FOXO3, and expression of Bcl2 to assess the role of GSH in promoting cell survival in response to ischemic injury. Based on our results, we suggest that GSH might improve the pathogenesis of ischemic stroke by attenuating cerebral infarction and cell death.
Files in This Item:
T201500438.pdf Download
DOI
10.1155/2015/426069
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Anatomy (해부학교실) > 1. Journal Papers
Yonsei Authors
Park, Joohyun(박주현) ORCID logo https://orcid.org/0000-0002-0897-4665
Song, Ju Hyun(송주현)
Lee, Jong Eun(이종은) ORCID logo https://orcid.org/0000-0001-6203-7413
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/139479
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