Effect of ischemic preconditioning on the expression of c-myb in the CA1 region of the gerbil hippocampus after ischemia/reperfusion injury

Document Type: Original Article


1 Department of Internal Medicine, School of Medicine, Kangwon National University, Chuncheon 200-701, South Korea

2 Department of Biomedical Science, Research Institute of Bioscience and Biotechnology, Hallym University, Chuncheon 200-702, South Korea

3 Pharmacology & Toxicology Department, Shinpoong Pharmaceutical Co., Ltd., Ansan 425-100, South Korea

4 Department of Neurobiology, School of Medicine, Kangwon National University, Chuncheon 200-701, South Korea

5 Department of Physiology, College of Medicine, Hallym University, Chuncheon 200-702, South Korea

6 Department of Emergency Medicine, School of Medicine, Kangwon National University, Chuncheon 200-701, South Korea

7 Department of Emergency Medicine, Chuncheon Sacred Heart Hospital, College of Medicine, Hallym University, Chuncheon 200-702, South Korea


Objective(s): In the present study, we investigated the effect of ischemic preconditioning (IPC) on c-myb immunoreactivity as well as neuronal damage/death after a subsequent lethal transient ischemia in gerbils.
Materials and Methods: IPC was subjected to a 2 min sublethal ischemia and a lethal transient ischemia was given 5 min transient ischemia. The animals in all of the groups were given recovery times of 1 day, 2 days and 5 days and we examined change in c-myb immunoreactivity as well as neuronal damage/death in the hippocampus induced by a lethal transient ischemia.
Results:A lethal transient ischemia induced a significant loss of cells in the stratum pyramidale (SP) of the hippocampal CA1 region at 5 days post-ischemia, and this insult showed that c-myb immunoreactivity in cells of the SP of the CA1 region was significantly decreased at 2 days post-ischemia and disappeared at 5 days post-ischemia. However, IPC effectively prevented the neuronal loss in the SP and showed that c-myb immunoreactivity was constitutively maintained in the SP after a lethal transient ischemia.
Conclusion: Our results show that a lethal transient ischemia significantly decreased c-myb immunoreactivity in the SP of the CA1 region and that IPC well preserved c-myb immunoreactivity in the SP of the CA1 region. We suggest that the maintenance of c-myb might be related with IPC-mediated neuroprotection after a lethal ischemic insult.


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