Effect of hyperthermia on calbindin-D 28k immunoreactivity in the hippocampal formation following transient global cerebral ischemia in gerbils.
Effect of hyperthermia on calbindin-D 28k immunoreactivity in the hippocampal formation following transient global cerebral ischemia in gerbils.
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DOI：
10.4103/1673-5374.215256
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发表时间：
2017-09
影响因子：
6.1
通讯作者：
Kim YH
中科院分区：
文献类型：
--
作者：
Lee JC;Cho JH;Lee TK;Kim IH;Won MH;Cho GS;Shin BN;Hwang IK;Park JH;Ahn JH;Kang IJ;Lee YJ;Kim YH
Calbindin D-28K (CB) 是一种 Ca2+ 结合蛋白，可维持 Ca2+ 稳态并保护神经元免受各种损伤。体温过高会加剧缺血性损伤造成的脑损伤。然而，关于 CB 在缺血性损伤期间高温条件下大脑中的作用的报道很少。我们使用沙鼠神经元核 (NeuN) 和 CB 的免疫组织化学以及 Fluoro-Jade B 组织荧光染色研究了短暂性全脑缺血对 CB 免疫反应性以及高温条件下海马结构神经元损伤的影响。在短暂性缺血之前和期间诱导高热（39.5±0.2°C）30分钟。 Hyperthermic ischemia resulted in neuronal 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.此外，高温缺血在缺血后 1、2、5 天显着降低受损或死亡神经元的 CB 免疫反应性。 In brief, hyperthermic condition produced more extensive and severer neuronal damage/death, and reduced CB immunoreactivity in the hippocampus following transient global cerebral ischemia.目前的研究结果表明，CB免疫反应性降低的程度可能与缺血性损伤后各种神经元损伤/死亡以及相应区域有关。
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 investigated 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 neuronal 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 immunoreactivity 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 immunoreactivity might be related with various neuronal damage/death overtime and corresponding areas after ischemic insults.
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影响因子：
8.2
作者：
Li, Ming-hua;Inoue, Koichi;Si, Hong-fang;Xiong, Zhi-gang
通讯作者：
Xiong, Zhi-gang
影响因子：
4.4
作者：
Kim, Min Joung;Cho, Jun Hwi;Lee, Jae-Chul
通讯作者：
Lee, Jae-Chul
影响因子：
3.3
作者：
Klapstein, GJ;Vietla, S;Mody, I
通讯作者：
Mody, I
影响因子：
3.4
作者：
HALASY, K;MIETTINEN, R;FREUND, TF
通讯作者：
FREUND, TF
影响因子：
4.4
作者：
Lee, Young Joo;Yan, Bing Chun;Cho, Jun Hwi
通讯作者：
Cho, Jun Hwi