In Hye Kim1, Jae-Chul Lee1, Joon Ha Park1, Ji Hyeon Ahn1, Jeong-Hwi Cho1, Bai Hui Chen2, Bich Na Shin2, Bing Chun Yan3, Dong Rueol Ryu4, Seongkweon Hong5, Jun Hwi Cho6, Yun Lyul Lee2, Young-Myeong Kim7, Byung-Ryul Cho4, Moo-Ho Won1. 1. a Department of Neurobiology, School of Medicine , Kangwon National University , Chuncheon , South Korea. 2. b Department of Physiology, College of Medicine , Hallym University , Chuncheon , South Korea. 3. c Institute of Integrative Traditional & Western Medicine, Medical College , Yangzhou University , China. 4. d Department of Internal Medicine, School of Medicine , Kangwon National University , Chuncheon , South Korea. 5. e Department of Surgery, School of Medicine , Kangwon National University , Chuncheon , South Korea. 6. f Department of Emergency Medicine, School of Medicine , Kangwon National University , Chuncheon , South Korea. 7. g Department of Molecular and Cellular Biochemistry, School of Medicine , Kangwon National University , Chuncheon , South Korea.
Abstract
OBJECTIVES: Ischaemic preconditioning (IPC) can increase ischaemic tolerance of the central nervous system (CNS) to a subsequent longer or lethal period of transient ischaemia. In this study, we examined neuroprotective effects of time intervals after IPC against ischaemic insult in the hippocampus. METHODS: Animals were randomly assigned to six groups; sham-operated-group, ischaemia-operated-group, and three IPC (12 hours, 1- and 2-day intervals after IPC) plus ischaemia-groups (IPC-12 hour, 1 and 2-day interval-ischaemia-operated-groups). For neuroprotection, we carried out cresyl violet (CV) staining neuronal nuclei (NeuN) immunohistochemistry and Fluoro-Jade B histofluorescence staining. In addition, we examined gliosis using immunohistochemistry for GFAP (a marker for astrocytes) and Iba-1 (a marker for microglia). RESULTS: A significant loss of neurons was observed in the stratum pyramidale (SP) of the hippocampal CA1 region (CA1) in the ischaemia-operated-group and IPC-12 hours interval-ischaemia-operated-groups. In the IPC-1 day interval-ischaemia-operated-group, CA1 pyramidal neurons were well protected from ischaemic insult; the neuroprotective effect in the IPC-2 day interval-ischaemia-operated-group was less than that in the IPC-1 day interval-ischaemia-operated-group. On the other hand, we observed changes in glial cells (astrocytes and microglia) in the CA1 of all groups. The distribution pattern of glial cells only in the IPC-1 day interval-ischaemia-operated-group was similar to that in the sham-group. CONCLUSION: In brief, our findings indicate that 1 day after IPC displays a mighty neuroprotection and shows an inhibition of glial activation in the CA1 induced by transient ischaemic insult.
OBJECTIVES: Ischaemic preconditioning (IPC) can increase ischaemic tolerance of the central nervous system (CNS) to a subsequent longer or lethal period of transient ischaemia. In this study, we examined neuroprotective effects of time intervals after IPC against ischaemic insult in the hippocampus. METHODS: Animals were randomly assigned to six groups; sham-operated-group, ischaemia-operated-group, and three IPC (12 hours, 1- and 2-day intervals after IPC) plus ischaemia-groups (IPC-12 hour, 1 and 2-day interval-ischaemia-operated-groups). For neuroprotection, we carried out cresyl violet (CV) staining neuronal nuclei (NeuN) immunohistochemistry and Fluoro-Jade B histofluorescence staining. In addition, we examined gliosis using immunohistochemistry for GFAP (a marker for astrocytes) and Iba-1 (a marker for microglia). RESULTS: A significant loss of neurons was observed in the stratum pyramidale (SP) of the hippocampal CA1 region (CA1) in the ischaemia-operated-group and IPC-12 hours interval-ischaemia-operated-groups. In the IPC-1 day interval-ischaemia-operated-group, CA1 pyramidal neurons were well protected from ischaemic insult; the neuroprotective effect in the IPC-2 day interval-ischaemia-operated-group was less than that in the IPC-1 day interval-ischaemia-operated-group. On the other hand, we observed changes in glial cells (astrocytes and microglia) in the CA1 of all groups. The distribution pattern of glial cells only in the IPC-1 day interval-ischaemia-operated-group was similar to that in the sham-group. CONCLUSION: In brief, our findings indicate that 1 day after IPC displays a mighty neuroprotection and shows an inhibition of glial activation in the CA1 induced by transient ischaemic insult.
Entities:
Keywords:
Delayed neuronal death; Gliosis; Ischaemia–reperfusion; Neuroprotection; Pyramidal neurons; Time intervals after IPC