2006Zhongguo yaolixue tongbaoRequires access

The expression and role of ERK and JNK in cerebral ischemic preconditioning in gerbil

Yaoqi Wang, Jun Li

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Abstract

Aim To explore the expression and role of ERK and JNK in cerebral ischemic preconditioning in gerbil.Methods Forebrain ischemia was induced by occlusion of bilateral carotid arteries.Gerbils were randomly divided into sham group(SH),ischemic-preconditioning control group(IC),ischemic-preconditioning group(IP),ischemia-reperfusion group(IR).The gerbils were killed in 15 min,2,4,6 h,1,3,5 and 7 d in each group following reperfusion.Open field test was used to examine the behavioral deficit in the due time.The number of surviving and apoptosis neurons in hippocampal CA1/3 region was counted,and the activity of p-ERK and p-JNK in hippocampus was detected using SP immunocytochemical technique.Results The behavioral mark and the number of apoptosis neurons in hippocampal CA1 region in group IP were much less than that in group IR(P0.01),no expression of p-ERK was detected in CA1 region in each group,but the levels of p-JNK were markedly expressed in CA1 region,especially at 1d after reperfusion.The levels of p-JNK in CA1 region were much lower in group IP than that in group IR(P0.01),and the expression of p-ERK in CA3 region was significantly enhanced in IP group(vs IR,P0.05,P0.01).Conclusion Cerebral ischemia caused p-ERK and p-JNK to be expressed differently in gerbil hippocampal regions.Ischemic-preconditioning may protect gerbil hippocampal neurons from ischemic injury through inhibiting the expression of p-JNK in CA1 region and enhancing the activity of p-ERK in CA3 region.

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Aim To explore the expression and role of ERK and JNK in cerebral ischemic preconditioning in gerbil.Methods Forebrain ischemia was induced by occlusion of bilateral carotid arteries.Gerbils were randomly divided into sham group(SH),ischemic-preconditioning control group(IC),ischemic-preconditioning group(IP),ischemia-reperfusion group(IR).The gerbils were killed in 15 min,2,4,6 h,1,3,5 and 7 d in each group following reperfusion.Open field test was used to examine the behavioral deficit in the due time.The number of surviving and apoptosis neurons in hippocampal CA1/3 region was counted,and the activity of p-ERK and p-JNK in hippocampus was detected using SP immunocytochemical technique.Results The behavioral mark and the number of apoptosis neurons in hippocampal CA1 region in group IP were much less than that in group IR(P0.01),no expression of p-ERK was detected in CA1 region in each group,but the levels of p-JNK were markedly expressed in CA1 region,especially at 1d after reperfusion.The levels of p-JNK in CA1 region were much lower in group IP than that in group IR(P0.01),and the expression of p-ERK in CA3 region was significantly enhanced in IP group(vs IR,P0.05,P0.01).Conclusion Cerebral ischemia caused p-ERK and p-JNK to be expressed differently in gerbil hippocampal regions.Ischemic-preconditioning may protect gerbil hippocampal neurons from ischemic injury through inhibiting the expression of p-JNK in CA1 region and enhancing the activity of p-ERK in CA3 region.

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Available abstract

Aim To explore the expression and role of ERK and JNK in cerebral ischemic preconditioning in gerbil.Methods Forebrain ischemia was induced by occlusion of bilateral carotid arteries.Gerbils were randomly divided into sham group(SH),ischemic-preconditioning control group(IC),ischemic-preconditioning group(IP),ischemia-reperfusion group(IR).The gerbils were killed in 15 min,2,4,6 h,1,3,5 and 7 d in each group following reperfusion.Open field test was used to examine the behavioral deficit in the due time.The number of surviving and apoptosis neurons in hippocampal CA1/3 region was counted,and the activity of p-ERK and p-JNK in hippocampus was detected using SP immunocytochemical technique.Results The behavioral mark and the number of apoptosis neurons in hippocampal CA1 region in group IP were much less than that in group IR(P0.01),no expression of p-ERK was detected in CA1 region in each group,but the levels of p-JNK were markedly expressed in CA1 region,especially at 1d after reperfusion.The levels of p-JNK in CA1 region were much lower in group IP than that in group IR(P0.01),and the expression of p-ERK in CA3 region was significantly enhanced in IP group(vs IR,P0.05,P0.01).Conclusion Cerebral ischemia caused p-ERK and p-JNK to be expressed differently in gerbil hippocampal regions.Ischemic-preconditioning may protect gerbil hippocampal neurons from ischemic injury through inhibiting the expression of p-JNK in CA1 region and enhancing the activity of p-ERK in CA3 region.

Key concepts: Gerbil, Hippocampal formation, Ischemic preconditioning, Hippocampus, Ischemia, MAPK/ERK pathway, Apoptosis, p38 mitogen-activated protein kinases

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