Changes of Translocation of Heterogeneous Nuclear Ribonulcleoprotein A2/B1 of Brain Cortex after Cerebral Ischemic Reperfusion in Rats
Hangyan Wang
Abstract
Hangyan Wang
Abstract
Objective To investigate the dynamic changes of translocation of heterogeneous nuclear ribonulcleoprotein A2/B1(hnRNP A2/B1) in rats after brain cortex and its relation to the time of reperfusion.Methods A total of 30 male SD rats were randomly divided into 6 groups:sham operated group without ischemia(n=5) and other 5 groups with 2 h ischemic followed by reperfusion at different times(3 h,6 h,12 h,24 h,48 h;n=5 in each group).Focal cerebral ischemia reperfusion models were induced by using the right middle cerebral artery(MCA) of SD rats and occluded for 2 h by the use of an intralaminal filament and recirculation was instituted for 3 h,6 h,12 h,24 h,48 h.Sham operated rats were not subjected to middle cerebral artery occlusion/reperfusion served as controls.Immunohistochemistry technique was employed to examine localization changes in hnRNP A2/B1 in rat cerebral cortex(including cingulum cortex,striate cortex,temporal cortex and piriform cortex) after ischemical reperfusion injury.Morphological changes in neuronal cells were identified in cerebral cortex after ischemic reperfusion injury by Nissl′s staining method.Results 1.Immunohistochemistry observations demonstrated a nucleoplasmic localization of hnRNP A2/B1 in cerebral cortex in sham operated group.After 3 h,6 h,12 h,24 h,48 h of ischemia reperfusion in cerebral cortex,hnRNP A2/B1 were observed to translocate from nuclear to cytoplasm and neuronal dendrite,which rose first and then fell.Compared with the sham operated group,translocation of hnRNP A2/B1 from nucleus to cytoplasm and even to neurons was observed in cerebral cortex at 3 h of ischemic reperfusion(P0.01) and continuously increased at 12 h(P0.01),reached a peak at 24 h(P0.01) of reperfusion.After 48 h after ischemic reperfusion,the number of hnRNP A2/B1 translocation neurons reduced dramatically to the minimum level.2.With contrast to the sham operated group,neuronal damage was relatively severe in the cerebral cortex in ischemic reperfusion groups.After 24 h reperfusion,neuronal cells death was delayed significantly in the whole cortex.Conclusion HnRNP A2/B1 might be involved in regulating brain ischemical reperfusion injury on post-transcriptional level.
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Objective To investigate the dynamic changes of translocation of heterogeneous nuclear ribonulcleoprotein A2/B1(hnRNP A2/B1) in rats after brain cortex and its relation to the time of reperfusion.Methods A total of 30 male SD rats were randomly divided into 6 groups:sham operated group without ischemia(n=5) and other 5 groups with 2 h ischemic followed by reperfusion at different times(3 h,6 h,12 h,24 h,48 h;n=5 in each group).Focal cerebral ischemia reperfusion models were induced by using the right middle cerebral artery(MCA) of SD rats and occluded for 2 h by the use of an intralaminal filament and recirculation was instituted for 3 h,6 h,12 h,24 h,48 h.Sham operated rats were not subjected to middle cerebral artery occlusion/reperfusion served as controls.Immunohistochemistry technique was employed to examine localization changes in hnRNP A2/B1 in rat cerebral cortex(including cingulum cortex,striate cortex,temporal cortex and piriform cortex) after ischemical reperfusion injury.Morphological changes in neuronal cells were identified in cerebral cortex after ischemic reperfusion injury by Nissl′s staining method.Results 1.Immunohistochemistry observations demonstrated a nucleoplasmic localization of hnRNP A2/B1 in cerebral cortex in sham operated group.After 3 h,6 h,12 h,24 h,48 h of ischemia reperfusion in cerebral cortex,hnRNP A2/B1 were observed to translocate from nuclear to cytoplasm and neuronal dendrite,which rose first and then fell.Compared with the sham operated group,translocation of hnRNP A2/B1 from nucleus to cytoplasm and even to neurons was observed in cerebral cortex at 3 h of ischemic reperfusion(P0.01) and continuously increased at 12 h(P0.01),reached a peak at 24 h(P0.01) of reperfusion.After 48 h after ischemic reperfusion,the number of hnRNP A2/B1 translocation neurons reduced dramatically to the minimum level.2.With contrast to the sham operated group,neuronal damage was relatively severe in the cerebral cortex in ischemic reperfusion groups.After 24 h reperfusion,neuronal cells death was delayed significantly in the whole cortex.Conclusion HnRNP A2/B1 might be involved in regulating brain ischemical reperfusion injury on post-transcriptional level.
Key concepts: Cortex (anatomy), Cerebral cortex, Middle cerebral artery, Ischemia, Piriform cortex, Nissl body, Reperfusion injury, Anatomy