2012•Journal of Apoplexy and Nervous DiseasesRequires access

Mild hypothermia affects c-Jun expression in hippocampal CA_1 subfield following globle cerebral ischemia

Li-xiu Han

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Abstract

Objective To investigate the neuroprotection of mild hypothermia on the hippocampal CA1 neurons following global cerebral ischemia/ reperfusion in SD rat models,and to explore the possible underlying mechanism.Methods Global cerebral ischemia/reperfusion model was produced by 4-VO method.Rats were randomly divided into 3 groups:sham(SH)group,normothermic ischemic reperfusion(IR)group and hypothermic ischemic reperfusion(HIR)group.15min after the cerebral ischemia,the reperfusion was performed for 6h,12h,1d and 3d.The changes of hippocampal neurons morphology in the CA1 subfield were observed by hematoxylin-eosin(HE)staining and the neuron apoptosis was detected by TUNEL method.The c-Jun expression was detected by immuno-blotting test at each time point.Results Neurons in hippocampal CA1 subfield of IR group were observed abnormal appearance by HE staining with pyknotic nucleus,shrunken shape and destroyed-former lines on 1d after ischemia/reperfusion,especially on 3d after ischemia/reperfusion.Compared with IR group,the number of normal cells increased in hippocampal CA1 subfield of HIR group at 12h,1d and 3d(P0.05).Compared with SH group,markedly TUNEL positive cell increased in hippocampal CA1 subfield of IR group at 6h,especially on 1d(P0.01).The number of apoptotic cells in hippocampal CA1 subfield of HIR group were less than that of IR group at corresponding time(P0.01).In CA1 subfield of IR group after global cerebral ischemia/ reperfusion,c-Jun peaked at 12h and continued until 3d,and the espression of c-Jun significantly decreased in hippocampal CA1 subfield of HIR group at corresponding time(P0.01).Conclusion Mild hypothermia decreases number of apoptotic cells in hippocampal CA1 subfield by inhibiting the overexpression of c-Jun and protect neurons.

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Objective To investigate the neuroprotection of mild hypothermia on the hippocampal CA1 neurons following global cerebral ischemia/ reperfusion in SD rat models,and to explore the possible underlying mechanism.Methods Global cerebral ischemia/reperfusion model was produced by 4-VO method.Rats were randomly divided into 3 groups:sham(SH)group,normothermic ischemic reperfusion(IR)group and hypothermic ischemic reperfusion(HIR)group.15min after the cerebral ischemia,the reperfusion was performed for 6h,12h,1d and 3d.The changes of hippocampal neurons morphology in the CA1 subfield were observed by hematoxylin-eosin(HE)staining and the neuron apoptosis was detected by TUNEL method.The c-Jun expression was detected by immuno-blotting test at each time point.Results Neurons in hippocampal CA1 subfield of IR group were observed abnormal appearance by HE staining with pyknotic nucleus,shrunken shape and destroyed-former lines on 1d after ischemia/reperfusion,especially on 3d after ischemia/reperfusion.Compared with IR group,the number of normal cells increased in hippocampal CA1 subfield of HIR group at 12h,1d and 3d(P0.05).Compared with SH group,markedly TUNEL positive cell increased in hippocampal CA1 subfield of IR group at 6h,especially on 1d(P0.01).The number of apoptotic cells in hippocampal CA1 subfield of HIR group were less than that of IR group at corresponding time(P0.01).In CA1 subfield of IR group after global cerebral ischemia/ reperfusion,c-Jun peaked at 12h and continued until 3d,and the espression of c-Jun significantly decreased in hippocampal CA1 subfield of HIR group at corresponding time(P0.01).Conclusion Mild hypothermia decreases number of apoptotic cells in hippocampal CA1 subfield by inhibiting the overexpression of c-Jun and protect neurons.

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Available abstract

Objective To investigate the neuroprotection of mild hypothermia on the hippocampal CA1 neurons following global cerebral ischemia/ reperfusion in SD rat models,and to explore the possible underlying mechanism.Methods Global cerebral ischemia/reperfusion model was produced by 4-VO method.Rats were randomly divided into 3 groups:sham(SH)group,normothermic ischemic reperfusion(IR)group and hypothermic ischemic reperfusion(HIR)group.15min after the cerebral ischemia,the reperfusion was performed for 6h,12h,1d and 3d.The changes of hippocampal neurons morphology in the CA1 subfield were observed by hematoxylin-eosin(HE)staining and the neuron apoptosis was detected by TUNEL method.The c-Jun expression was detected by immuno-blotting test at each time point.Results Neurons in hippocampal CA1 subfield of IR group were observed abnormal appearance by HE staining with pyknotic nucleus,shrunken shape and destroyed-former lines on 1d after ischemia/reperfusion,especially on 3d after ischemia/reperfusion.Compared with IR group,the number of normal cells increased in hippocampal CA1 subfield of HIR group at 12h,1d and 3d(P0.05).Compared with SH group,markedly TUNEL positive cell increased in hippocampal CA1 subfield of IR group at 6h,especially on 1d(P0.01).The number of apoptotic cells in hippocampal CA1 subfield of HIR group were less than that of IR group at corresponding time(P0.01).In CA1 subfield of IR group after global cerebral ischemia/ reperfusion,c-Jun peaked at 12h and continued until 3d,and the espression of c-Jun significantly decreased in hippocampal CA1 subfield of HIR group at corresponding time(P0.01).Conclusion Mild hypothermia decreases number of apoptotic cells in hippocampal CA1 subfield by inhibiting the overexpression of c-Jun and protect neurons.

Key concepts: Hippocampal formation, TUNEL assay, Neuroprotection, Ischemia, Hippocampus, Apoptosis, H&E stain, Anesthesia

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