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EXPERIMENTAL STUDY ON GLIAL RESPONSES TO NEONATAL HYPOXIC/ISCHEMIC ENCEPHALOPATYH

神经胶质细胞对新生儿缺氧/缺血性脑病反应的实验研究

基本信息

批准号：
06670785
负责人：
OHNO Masaki
金额：
$ 1.09万
依托单位：
Shiga University of Medical Science
依托单位国家：
日本
项目类别：
Grant-in-Aid for General Scientific Research (C)
财政年份：
1994
资助国家：
日本
起止时间：
1994 至 1995
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-06670785/
关键词：
HYPOXIC ISCHEMIC ENCEPHALOPATHY NEONATE GLIA MICROGLIA PDGF アストログリア神経栄養因子

项目摘要

In the first year of the research project, we have investigated the cellular responses to hypoxic/ischemic encephalopathy in the neonatal rats. Left common carotid artery of the 7-day-old rats was ligated, and the pups were placed in a hypoxic chamber. The glial responses were examined using the immunocytochemistry. The results indicate that developing microglia are the first and principle glial element that responds to hypoxic/ischemic injury during the neonatal period. The astrocyte respose occurs later. These glial responses may play important roles in the neuronal degeneration and/or tissue remodeling.In the second year of the research project, expressions of platelet-derived growth factor (PDGF) B-chain and PDGF beta-receptor have been investigated in the immature brains with hypoxic/ischemic injury. The expressions of PDGF B-chain and its specific receptor protein and mRNA were examined using an immunocytochemistry and a northern analysis, respcetively. The results indicate that neonatal hypoxic/ischemic insult induces the upregulation of PDGF B-chain and beta-receptor expressions in neurons immediately after hypoxia. This upregulation, however, was tentative in most neurons. Sublethal damage on neurons in peri-infarct areas induces the sustained and long-term upregulations of PDGF B-chain and beta-receptor. PDGF B-chain molecules may act as a neuroprotective factor in developing brain with hypoxic/ischemic injury through autocrine and paracrine mechanisms.

在研究项目的第一年，我们研究了新生大鼠缺氧缺血性脑病的细胞反应。结扎7日龄大鼠的左颈总动脉，并将幼鼠置于低氧室中。免疫细胞化学法检测胶质细胞反应。结果表明，发展中的小胶质细胞是第一个和主要的胶质细胞的元素，在新生儿期的缺氧/缺血性损伤。星形胶质细胞的反应较晚。本课题的第二年研究了血小板源性生长因子（platelet-derived growth factor，PDGF）B链和PDGF β受体在未成熟脑缺氧缺血损伤中的表达。采用免疫细胞化学和北方分析法检测PDGF B链及其特异性受体蛋白和mRNA的表达。结果表明，新生儿缺氧/缺血损伤诱导PDGF B链和β受体表达的上调后，立即在缺氧。然而，这种上调在大多数神经元中是暂时的。脑梗死周围神经元的亚致死性损伤诱导PDGF B链和β受体的持续和长期上调。PDGF B链分子可能通过自分泌和旁分泌机制在发育中的脑缺氧缺血损伤中发挥神经保护作用。