Bcl-2 and Bax expression in rat hippocampus after global cerebral ischemia-reperfusion
Jiangquan Han
Abstract
Jiangquan Han
Abstract
Objective To investigate the expression of Bcl-2/Bax in hippocampus after cerebral ischemia-reperfusion.Methods 48 healthy SD rats were randomly divided into 2 groups,including sham operation(SO) group(n=24) and I/R group(n=24).The model of global cerebral ischemia/reperfusion injury was produced by simple Pulsinelli-Brierley's four arteries occlusion method.Bcl-2 and Bax expression in rat hippocampal CA1 pyramidal cells were detected with imunolistochemestry SABC assay.HE staining was performed to detect the number of surviving neurons.Results In I/R group,the average gray value of Bcl-2 began to decrease at 3h after reperfusion.The average gray value of Bax began to decrease at 3h after reperfusion,The peak was at 24h,and then gradually increased at 48h.The number of surviving neurons reduced with the extension of reperfusion(P0.01).Conclusions After global cerebral ischemia/reperfusion,neurons apoptosis is regulated by Bcl-2 and Bax.
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Objective To investigate the expression of Bcl-2/Bax in hippocampus after cerebral ischemia-reperfusion.Methods 48 healthy SD rats were randomly divided into 2 groups,including sham operation(SO) group(n=24) and I/R group(n=24).The model of global cerebral ischemia/reperfusion injury was produced by simple Pulsinelli-Brierley's four arteries occlusion method.Bcl-2 and Bax expression in rat hippocampal CA1 pyramidal cells were detected with imunolistochemestry SABC assay.HE staining was performed to detect the number of surviving neurons.Results In I/R group,the average gray value of Bcl-2 began to decrease at 3h after reperfusion.The average gray value of Bax began to decrease at 3h after reperfusion,The peak was at 24h,and then gradually increased at 48h.The number of surviving neurons reduced with the extension of reperfusion(P0.01).Conclusions After global cerebral ischemia/reperfusion,neurons apoptosis is regulated by Bcl-2 and Bax.
Key concepts: Medicine, Apoptosis, Hippocampal formation, Ischemia, Reperfusion injury, Hippocampus, Immunohistochemistry, Anesthesia