2014Chinese Journal of NeuromedicineRequires access

Effects of inhibition of adenosine monophosphate-activated protein kinase activity on neuronal apoptosis in mice after cerebral ischemia reperfusion injury

Zhanbo Wang, Yi Zhu, Hui Dang, Juan Bu, Jing Sha, Jing Yan, Shan-jiang Ai

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Abstract

Objective To investigate the effects of inhibition of adenosine monophosphate-activated protein kinase (AMPK) activity on neuronal apoptosis in mice after cerebral ischemia reperfusion injury.Methods Fifty-four male C57BL/6 mice were randomly divided into three groups (n=18):sham-operated group,ischemia reperfusion group and ischemia reperfusion therapy group.Mice models of middle cerebral artery occlusion (MCAO) in the later two groups were made by insertion of a thread through intemal carotid artery.Compound C was injected intraperitoneally in ischemia reperfusion therapy group when the thread was inserted.The same volume of saline was given to the sham-operated group and ischemia reperfusion group at the same time to intraperitonel injection.The Cytochrome C (Cy C) expression and neuronal apoptosis were observed by immunohistochemical staining and TUNEL 24 h after cerebral ischemia reperfusion injury.Results As compared with that in the ischemia reperfusion group,the histopathological damage was reduced in the hippocampal CA1 region of mice in the ischemia reperfusion therapy group; Cyt C positive cells in the two groups were (28.86±9.65)/field and (13.33±2.75)/field,respectively.TUNEL positive cells in the two groups were (67.14±8.55)/HP and (74.57±6.77)/HP,with significant difference (P<0.05).Conclusion Inhibition of AMPK activity can decrease cerebral ischemia reperfusion injury,which is problely by lowering the Cyt C expression to decrease the neuronal apoptosis in mice. Key words: Cerebral ischemia/reperfusion;  Cytochrome C;  Neuronal apoptosis;  Adenosine monophosphate-activated protein kinase

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Objective To investigate the effects of inhibition of adenosine monophosphate-activated protein kinase (AMPK) activity on neuronal apoptosis in mice after cerebral ischemia reperfusion injury.Methods Fifty-four male C57BL/6 mice were randomly divided into three groups (n=18):sham-operated group,ischemia reperfusion group and ischemia reperfusion therapy group.Mice models of middle cerebral artery occlusion (MCAO) in the later two groups were made by insertion of a thread through intemal carotid artery.Compound C was injected intraperitoneally in ischemia reperfusion therapy group when the thread was inserted.The same volume of saline was given to the sham-operated group and ischemia reperfusion group at the same time to intraperitonel injection.The Cytochrome C (Cy C) expression and neuronal apoptosis were observed by immunohistochemical staining and TUNEL 24 h after cerebral ischemia reperfusion injury.Results As compared with that in the ischemia reperfusion group,the histopathological damage was reduced in the hippocampal CA1 region of mice in the ischemia reperfusion therapy group; Cyt C positive cells in the two groups were (28.86±9.65)/field and (13.33±2.75)/field,respectively.TUNEL positive cells in the two groups were (67.14±8.55)/HP and (74.57±6.77)/HP,with significant difference (P<0.05).Conclusion Inhibition of AMPK activity can decrease cerebral ischemia reperfusion injury,which is problely by lowering the Cyt C expression to decrease the neuronal apoptosis in mice. Key words: Cerebral ischemia/reperfusion;  Cytochrome C;  Neuronal apoptosis;  Adenosine monophosphate-activated protein kinase

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Available abstract

Objective To investigate the effects of inhibition of adenosine monophosphate-activated protein kinase (AMPK) activity on neuronal apoptosis in mice after cerebral ischemia reperfusion injury.Methods Fifty-four male C57BL/6 mice were randomly divided into three groups (n=18):sham-operated group,ischemia reperfusion group and ischemia reperfusion therapy group.Mice models of middle cerebral artery occlusion (MCAO) in the later two groups were made by insertion of a thread through intemal carotid artery.Compound C was injected intraperitoneally in ischemia reperfusion therapy group when the thread was inserted.The same volume of saline was given to the sham-operated group and ischemia reperfusion group at the same time to intraperitonel injection.The Cytochrome C (Cy C) expression and neuronal apoptosis were observed by immunohistochemical staining and TUNEL 24 h after cerebral ischemia reperfusion injury.Results As compared with that in the ischemia reperfusion group,the histopathological damage was reduced in the hippocampal CA1 region of mice in the ischemia reperfusion therapy group; Cyt C positive cells in the two groups were (28.86±9.65)/field and (13.33±2.75)/field,respectively.TUNEL positive cells in the two groups were (67.14±8.55)/HP and (74.57±6.77)/HP,with significant difference (P<0.05).Conclusion Inhibition of AMPK activity can decrease cerebral ischemia reperfusion injury,which is problely by lowering the Cyt C expression to decrease the neuronal apoptosis in mice. Key words: Cerebral ischemia/reperfusion;  Cytochrome C;  Neuronal apoptosis;  Adenosine monophosphate-activated protein kinase

Key concepts: Ischemia, TUNEL assay, Reperfusion injury, Medicine, AMPK, Apoptosis, Adenosine, Anesthesia

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