Impact of hyperthermia before and during ischemia-reperfusion on neuronal damage and gliosis in the gerbil hippocampus induced by transient cerebral ischemia
Impact of hyperthermia before and during ischemia-reperfusion on neuronal damage and gliosis in the gerbil hippocampus induced by transient cerebral ischemia
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DOI：
10.1016/j.jns.2014.11.015
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发表时间：
2015-01-15
影响因子：
4.4
通讯作者：
Lee, Jae-Chul
中科院分区：
文献类型：
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作者：
Kim, Min Joung;Cho, Jun Hwi;Lee, Jae-Chul
高温会加重脑缺血造成的脑损伤。本研究采用甲酚紫染色、NeuN免疫组化和Fluoro-Jade B组织荧光染色，研究了缺血再灌注前和缺血再灌注中高温对沙鼠短暂性脑缺血后海马神经元损伤和胶质细胞变化的影响。将动物随机分为4组：(1)正常母亲血症假手术组（正常母亲血症+假手术组）；(2)正常体温缺血手术动物（正常体温+缺血组）；(3)热疗假手术动物（热疗+假手术组）；(4)缺血手术热疗动物（热疗+缺血组）。在缺血再灌注之前和期间，将沙鼠暴露在连接直肠热敏电阻的加热垫中30分钟，以诱导热疗（39.5 +/- 0.2℃）。在正常体温+缺血组，缺血再灌注后5 d海马CM区锥体层（SP）出现明显的延迟性神经元死亡。热热+缺血组，缺血后1 d CM SP区出现神经元死亡，缺血后2 d CA2/3区SP区出现神经元死亡。此外，我们使用免疫组织化学检测了星形胶质细胞和小胶质细胞的激活情况，用于抗胶质纤维酸性蛋白（GFAP）和抗离子钙结合适配器分子1 （lba-1）。与正常体温+缺血组相比，高温+缺血组海马中gfap阳性星形胶质细胞和lba-1阳性小胶质细胞的激活时间明显提前和加速。基于我们的研究结果，我们认为在脑缺血损伤前的实验高温预条件会产生更广泛的神经元损伤和缺血海马的胶质细胞激活。(C) 2014 Elsevier B.V.版权所有
Hyperthermia can exacerbate the brain damage produced by ischemia. In the present study, we investigated the effects of hyperthermia before and during ischemia-reperfusion on neuronal damage and glial changes in the gerbil hippocampus following transient cerebral ischemia using cresyl violet staining, NeuN immunohisto-chemistry and Fluoro-Jade B histofluorescence staining. The animals were randomly assigned to 4 groups: (I) sham-operated animals with normothermia (normothermia + sham group); (2) ischemia-operated animals with normothermia (normothermia + ischemia group); (3) sham-operated animals with hyperthermia (hyperthermia + sham group); and (4) ischemia-operated animals with hyperthermia (hyperthermia + ischemia group). Hyperthermia (39.5 +/- 0.2 degrees C) was induced by exposing the gerbils to a heating pad connected to a rectal thermistor for 30 min before and during ischemia-reperfusion. In the normothermia + ischemia groups, a significant delayed neuronal death was observed in the stratum pyramidale (SP) of the hippocampal CM region (CM) 5 days after ischemia-reperfusion. In the hyperthermia + ischemia groups, neuronal death in the SP of the CM occurred at I day post-ischemia, and neuronal death was observed in the SP of the CA2/3 region at 2 days post-ischemia. In addition, we examined activations of astrocytes and microglia using immunohistochemistry for antiglial fibrillaiy acidic protein (GFAP) and anti-ionized calcium-binding adapter molecule 1 (lba-1). GFAP-positive astrocytes and lba-1-positive microglia in the ischemic hippocampus were activated much earlier and much more accelerated in the hyperthermia + ischemia groups than those in the normothermia + ischemia groups. Based on our findings, we suggest that an experimentally hyperthermic pre-condition before cerebral ischemic insult produces more extensive neuronal damage and glial activation in the ischemic hippocampus. (C) 2014 Elsevier B.V. All rights reserved.