The Akt signaling pathway contributes to postconditioning’s protection against stroke; the protection is associated with the MAPK and PKC pathways

• Published in: Journal of neurochemistry Vol. 105; no. 3; pp. 943 - 955
• Main Authors: Gao, Xuwen, Zhang, Hanfeng, Takahashi, Tetsuya, Hsieh, Jason, Liao, Janette, Steinberg, Gary K., Zhao, Heng
• Format: Journal Article
• Language: English
• Published: Oxford, UK Blackwell Publishing Ltd 01.05.2008; Blackwell
• Subjects: Akt; Animals; antagonists & inhibitors; Biochemistry; Biological and medical sciences; Brain; Brain - enzymology; Brain - physiopathology; Brain Ischemia; Brain Ischemia - enzymology; Brain Ischemia - physiopathology; Cell Death; Cell Death - physiology; Cell physiology; Cell Survival; Cell Survival - physiology; cerebral ischemia; Cytoprotection; Cytoprotection - physiology; Enzyme Activation; Enzyme Activation - physiology; Enzyme Inhibitors; Enzyme Inhibitors - pharmacology; enzymology; Fundamental and applied biological sciences. Psychology; Glycogen Synthase Kinase 3; Glycogen Synthase Kinase 3 - metabolism; Glycogen Synthase Kinase 3 beta; Ischemic Preconditioning; Kinases; Male; MAP Kinase Signaling System; MAP Kinase Signaling System - physiology; Medical sciences; metabolism; mitogen-activated protein kinase; Molecular and cellular biology; Neurology; pharmacology; Phosphatidylinositol 3-Kinases; Phosphatidylinositol 3-Kinases - metabolism; Phosphoinositide-3 Kinase Inhibitors; physiology; physiopathology; postconditioning; protein kinase C; Protein Kinase C - metabolism; Protein Kinase C-delta; Protein Kinase C-delta - metabolism; Protein Kinase C-epsilon; Protein Kinase C-epsilon - metabolism; Proto-Oncogene Proteins c-akt; Proto-Oncogene Proteins c-akt - metabolism; Rats; Rats, Sprague-Dawley; Signal transduction; Stroke; Stroke - enzymology; Stroke - physiopathology; Vascular diseases and vascular malformations of the nervous system; β‐catenin; Phosphoinositide; Phosphorylation; Protein kinase C; postconditioning; Infarct; Rat; Cardiovascular disease; Vascular disease; Signal transduction; β-catenin; Reperfusion; cerebral ischemia; Conditioning; Cerebrovascular disease; Nervous system diseases; Stroke; Enzyme; Transferases; Rodentia; Akt protein kinase; Mitogen-activated protein kinase; Akt; In vitro; Long term; Protein; Cerebral disorder; Vertebrata; Mammalia; Central nervous system disease; Brain ischemia

We previously reported that ischemic postconditioning with a series of mechanical interruptions of reperfusion reduced infarct volume 2 days after focal ischemia in rats. Here, we extend this data by examining long‐term protection and exploring underlying mechanisms involving the Akt, mitogen‐activa...