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缺血预处理对短暂性脑缺血后沙鼠海马 CA1 区 PDGF-BB 表达的影响。

Effects of ischemic preconditioning on PDGF-BB expression in the gerbil hippocampal CA1 region following transient cerebral ischemia.

机构信息

Department of Neurobiology, School of Medicine, Kangwon National University, Chuncheon, Gangwon 24341, Republic of Korea.

Department of Surgery, School of Medicine, Kangwon National University, Chuncheon, Gangwon 24341, Republic of Korea.

出版信息

Mol Med Rep. 2017 Aug;16(2):1627-1634. doi: 10.3892/mmr.2017.6799. Epub 2017 Jun 19.

DOI:10.3892/mmr.2017.6799
PMID:28627606
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5562056/
Abstract

Ischemic preconditioning (IPC) is induced by exposure to brief durations of transient ischemia, which results in ischemic tolerance to a subsequent longer or lethal period of ischemia. In the present study, the effects of IPC (2 min of transient cerebral ischemia) were examined on immunoreactivity of platelet‑derived growth factor (PDGF)‑BB and on neuroprotection in the gerbil hippocampal CA1 region following lethal transient cerebral ischemia (LTCI; 5 min of transient cerebral ischemia). IPC was subjected to a 2‑min sublethal ischemia and a LTCI was given 5‑min transient ischemia. The animals in all of the groups were given recovery times of 1, 2 and 5 days and change in PDGF‑BB immunoreactivity was examined as was the neuronal damage/death in the hippocampus induced by LTCI. LTCI induced a significant loss of pyramidal neurons in the hippocampal CA1 region 5 days after LTCI, and significantly decreased PDGF‑BB immunoreactivity in the CA1 pyramidal neurons from day 1 after LTCI. Conversely, IPC effectively protected the CA1 pyramidal neurons from LTCI and increased PDGF‑BB immunoreactivity in the CA1 pyramidal neurons post‑LTCI. In conclusion, the results demonstrated that LTCI significantly altered PDGF‑BB immunoreactivity in pyramidal neurons in the hippocampal CA1 region, whereas IPC increased the immunoreactivity. These findings indicated that PDGF‑BB may be associated with IPC‑mediated neuroprotection.

摘要

缺血预处理(IPC)是通过短暂缺血暴露诱导的,导致随后较长或致死性缺血期间的缺血耐受。在本研究中,研究了 IPC(短暂脑缺血 2 分钟)对致命性短暂脑缺血(LTCI;短暂脑缺血 5 分钟)后沙鼠海马 CA1 区血小板衍生生长因子(PDGF)-BB 免疫反应性和神经保护的影响。IPC 进行 2 分钟亚致死性缺血,LTCI 给予 5 分钟短暂性脑缺血。所有组的动物均给予 1、2 和 5 天的恢复时间,并检查 LTCI 诱导的 PDGF-BB 免疫反应性变化以及 LTCI 诱导的海马神经元损伤/死亡。LTCI 在 LTCI 后 5 天诱导海马 CA1 区锥体神经元明显丧失,并且从 LTCI 后第 1 天起 CA1 锥体神经元中的 PDGF-BB 免疫反应性显著降低。相反,IPC 有效地保护 CA1 锥体神经元免受 LTCI 的影响,并增加 LTCI 后 CA1 锥体神经元中的 PDGF-BB 免疫反应性。总之,结果表明 LTCI 显著改变了海马 CA1 区锥体神经元中 PDGF-BB 的免疫反应性,而 IPC 增加了其免疫反应性。这些发现表明 PDGF-BB 可能与 IPC 介导的神经保护有关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2144/5562056/0401185bde27/MMR-16-02-1627-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2144/5562056/1ad717a1108a/MMR-16-02-1627-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2144/5562056/bf5a1050d658/MMR-16-02-1627-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2144/5562056/41c7984c8b70/MMR-16-02-1627-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2144/5562056/ab6f665a1332/MMR-16-02-1627-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2144/5562056/0401185bde27/MMR-16-02-1627-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2144/5562056/1ad717a1108a/MMR-16-02-1627-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2144/5562056/bf5a1050d658/MMR-16-02-1627-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2144/5562056/41c7984c8b70/MMR-16-02-1627-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2144/5562056/ab6f665a1332/MMR-16-02-1627-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2144/5562056/0401185bde27/MMR-16-02-1627-g04.jpg

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