Suppr超能文献

血小板衍生生长因子诱导梗死耐受以对抗可逆性局灶性缺血

Induction of infarct tolerance by platelet-derived growth factor against reversible focal ischemia.

作者信息

Sakata M, Yanamoto H, Hashimoto N, Iihara K, Tsukahara T, Taniguchi T, Kikuchi H

机构信息

Laboratory for Cerebrovascular Disorders, National Cardiovascular Center Research Institute, 5-7-1 Fujishirodai, Suita, Osaka, 565, Japan.

出版信息

Brain Res. 1998 Feb 16;784(1-2):250-5. doi: 10.1016/s0006-8993(97)01345-0.

Abstract

Nerve growth factor, brain-derived neurotrophic factor, and other neurotrophic factors have been reported to have neuroprotective effects against global ischemia. To investigate whether the homodimer of platelet-derived growth factor B-chain (PDGF-BB) can protect neurons against focal temporary ischemia, PDGF-BB was administered to the rat brain for a prolonged period prior to, during, and after ischemia, since PDGF-BB protected rat neurons from global ischemia in our previous study. A total of 82 male Sprague-Dawley rats were used. Recombinant PDGF-BB, or saline was administered into the left neocortex via an implanted osmotic pump for 3 days (1.2 microg in total), 7 days (2 microgram or 4 microgram in total), or 14 days (4 microgram in total) pre-ischemia and 2 days post-ischemia. In an additional group, PDGF-BB (4 microgram in total) was administered for 14 days by osmotic pump and focal ischemia was induced after an additional 7-day interval following removal of the pump. Focal temporary ischemia was induced in the left MCA territory by bilateral CCA and MCA occlusion for 2 h. All rats were sacrificed 2 days after ischemia and the volume of cerebral infarct was analyzed using TTC staining. In a separate set of animals, regional cerebral blood flow (rCBF) was monitored by the hydrogen clearance method and laser Doppler flowmetry (LDF) of the neocortex after 14 days of intracerebral administration of PDGF-BB or saline. In the group receiving PDGF-BB (4 microgram in total) for 7 or 14 days pre-ischemia, there was a significant reduction of neocortical infarction compared to that in the control or saline-infused group. The size of cerebral infarct was smallest in the group that received PDGF-BB for 14 days, when ischemia was induced 7 days after removal of the pump. Regarding rCBF measurement, there were no significant differences in groups receiving PDGF-BB or saline infusion for 14 days. The potent neuroprotective effect of PDGF-BB on global ischemia was also demonstrated in the focal ischemia model. However, prolonged intracerebral infusion for 7 to 14 days was necessary to achieve a significant reduction of infarct volume. Neuroprotection was not due to increased collateral flow during ischemia.

摘要

据报道,神经生长因子、脑源性神经营养因子和其他神经营养因子对全脑缺血具有神经保护作用。为了研究血小板衍生生长因子B链(PDGF-BB)的同二聚体是否能保护神经元免受局灶性短暂性缺血损伤,由于在我们之前的研究中PDGF-BB可保护大鼠神经元免受全脑缺血损伤,因此在缺血前、缺血期间和缺血后对大鼠脑长期给予PDGF-BB。总共使用了82只雄性Sprague-Dawley大鼠。通过植入的渗透泵将重组PDGF-BB或生理盐水注入左侧新皮质,持续3天(总量1.2微克)、7天(总量2微克或4微克)或缺血前14天(总量4微克)以及缺血后2天。在另一组中,通过渗透泵给予PDGF-BB(总量4微克)14天,并在移除泵后再间隔7天诱导局灶性缺血。通过双侧颈总动脉和大脑中动脉闭塞2小时在左侧大脑中动脉区域诱导局灶性短暂性缺血。所有大鼠在缺血后2天处死,使用TTC染色分析脑梗死体积。在另一组动物中,在脑内给予PDGF-BB或生理盐水14天后,通过氢清除法和新皮质的激光多普勒血流仪(LDF)监测局部脑血流量(rCBF)。在缺血前接受PDGF-BB(总量4微克)7天或14天的组中,与对照组或注入生理盐水的组相比,新皮质梗死显著减少。在移除泵7天后诱导缺血时,接受PDGF-BB 14天的组脑梗死面积最小。关于rCBF测量,接受PDGF-BB或生理盐水注入14天的组之间没有显著差异。在局灶性缺血模型中也证实了PDGF-BB对全脑缺血具有强大的神经保护作用。然而,需要脑内长期输注7至14天才能使梗死体积显著减少。神经保护作用并非由于缺血期间侧支血流增加。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验