Effect of hyperthermia on calbindin-D 28k immunoreactivity in the hippocampal formation following transient global cerebral ischemia in gerbils  

作　　者：Jae-Chul Lee Jeong-Hwi Cho Tae-Kyeong Lee In Hye Kim Moo-Ho Won Geum-Sil Cho Bich-Na Shin In Koo Hwang Joon Ha Park Ji Hyeon Ahn Il Jun Kang Young Joo Lee Yang Hee Kim 

机构地区：[1]Department of Neurobiology, School of Medicine, Kangwon National University [2]Department of Pharmacology & Toxicology, Shinpoong Pharmaceutical Co., Ltd. [3]Department of Physiology, College of Medicine, Hallym University [4]Department of Anatomy and Cell Biology, College of Veterinary Medicine, and Research Institute for Veterinary Science, Seoul National University [5]Department of Biomedical Science, Research Institute of Bioscience and Biotechnology, Hallym University [6]Department of Food Science and Nutrition, Hallym University [7]Department of Emergency Medicine, Seoul Hospital, College of Medicine, Sooncheonhyang University [8]Department of Surgery, School of Medicine, Kangwon National University

出　　处：《Neural Regeneration Research》2017年第9期1458-1464,共7页中国神经再生研究（英文版）

基　　金：supported by the Biomedical Technology Development Program of the NRF funded by the Korean Government,MSIP(NRF-2015M3A9B6066835);by the Bio-Synergy Research Project(NRF-2015M3A9C4076322)of the Ministry of Science,ICT and Future Planning through the National Research Foundation

摘　　要：Calbindin D-28K （CB）, a Ca2＋-binding protein, maintains Ca2＋ homeostasis and protects neurons against various insults. Hyperthermia can exacerbate brain damage produced by ischemic insults. However, little is reported about the role of CB in the brain under hyperthermic condition during ischemic insults. We inves- tigated the effects of transient global cerebral ischemia on CB immunoreactivity as well as neuronal damage in the hippocampal formation under hyperthermic condition using immunohistochemistry for neuronal nuclei （NeuN） and CB, and Fluoro-Jade B histofluorescence staining in gerbils. Hyperthermia （39.5 ＋ 0.2~C） was induced for 30 minutes before and during transient ischemia. Hyperthermic ischemia resulted in neu- ronal damage/death in the pyramidal layer of CA1-3 area and in the polymorphic layer of the dentate gyrus at 1, 2, 5 days after ischemia. In addition, hyperthermic ischemia significantly decreaced CB immunoreac- tivity in damaged or dying neurons at 1, 2, 5 days after ischemia. In brief, hyperthermic condition produced more extensive and severer neuronal damage/death, and reduced CB immunoreactivity in the hippocampus following transient global cerebral ischemia. Present findings indicate that the degree of reduced CB immu- noreactivity might be related with various neuronal damage/death overtime and corresponding areas after ischemic insults.Calbindin D-28K （CB）, a Ca2＋-binding protein, maintains Ca2＋ homeostasis and protects neurons against various insults. Hyperthermia can exacerbate brain damage produced by ischemic insults. However, little is reported about the role of CB in the brain under hyperthermic condition during ischemic insults. We inves- tigated the effects of transient global cerebral ischemia on CB immunoreactivity as well as neuronal damage in the hippocampal formation under hyperthermic condition using immunohistochemistry for neuronal nuclei （NeuN） and CB, and Fluoro-Jade B histofluorescence staining in gerbils. Hyperthermia （39.5 ＋ 0.2~C） was induced for 30 minutes before and during transient ischemia. Hyperthermic ischemia resulted in neu- ronal damage/death in the pyramidal layer of CA1-3 area and in the polymorphic layer of the dentate gyrus at 1, 2, 5 days after ischemia. In addition, hyperthermic ischemia significantly decreaced CB immunoreac- tivity in damaged or dying neurons at 1, 2, 5 days after ischemia. In brief, hyperthermic condition produced more extensive and severer neuronal damage/death, and reduced CB immunoreactivity in the hippocampus following transient global cerebral ischemia. Present findings indicate that the degree of reduced CB immu- noreactivity might be related with various neuronal damage/death overtime and corresponding areas after ischemic insults.

关 键 词：nerve regeneration hyperthermic condition ischemia/reperfusion injury subregions of hippocampus delayed neuronal death calbindin D-28k neural regeneration 

分 类 号：R743[医药卫生—神经病学与精神病学]