Glutathione suppresses cerebral infarct volume and cell death after ischemic injury

Involvement of FOXO3 inactivation and Bcl2 expression

Juhyun Song, Joohyun Park, Yumi Oh, Jongeun Lee

Research output: Contribution to journalArticle

18 Citations (Scopus)

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.

Original languageEnglish
Article number426069
JournalOxidative Medicine and Cellular Longevity
Volume2015
DOIs
Publication statusPublished - 2015 Jan 1

Fingerprint

Cell death
Glutathione
Brain
Cerebral Infarction
Cell Death
Wounds and Injuries
Cell Survival
Claudin-5
Stroke
Cells
Oxidative stress
Middle Cerebral Artery Infarction
Scavenging
Reperfusion Injury
Phosphatidylinositol 3-Kinases
Reperfusion
Reactive Oxygen Species
Oxidative Stress
Blood
Ischemia

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Ageing
  • Cell Biology

Cite this

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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.",
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Glutathione suppresses cerebral infarct volume and cell death after ischemic injury : Involvement of FOXO3 inactivation and Bcl2 expression. / Song, Juhyun; Park, Joohyun; Oh, Yumi; Lee, Jongeun.

In: Oxidative Medicine and Cellular Longevity, Vol. 2015, 426069, 01.01.2015.

Research output: Contribution to journalArticle

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