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Neurological research · 2016

Time interval after ischaemic preconditioning affects neuroprotection and gliosis in the gerbil hippocampal CA1 region induced by transient cerebral ischaemia.

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Hye Kim In, Lee Jae-Chul, Ha Park Joon, Hyeon Ahn Ji, Cho Jeong-Hwi, Hui Chen Bai, Na Shin Bich, Chun Yan Bing, Rueol Ryu Dong, Hong Seongkweon, Hwi Cho Jun, Lyul Lee Yun, Kim Young-Myeong, Cho Byung-Ryul, Won Moo-Ho

Аннотация

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.

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