p38 MAPK Endogenous Inhibition Improves Neurological Deficits in Global Cerebral Ischemia/Reperfusion Mice.

IF 3.1 4区 医学 Q2 Medicine Neural Plasticity Pub Date : 2022-06-29 eCollection Date: 2022-01-01 DOI:10.1155/2022/3300327
Kun Hou, Zhi-Cheng Xiao, Hai-Long Dai
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引用次数: 3

Abstract

Cerebral ischemia/reperfusion (I/R) injury is a complex pathophysiological process that can lead to neurological function damage and the formation of cerebral infarction. The p38 MAPK pathway has attracted considerable attention in cerebral I/R injury (IRI), but little research has been carried out on its direct role in vivo. In this study, to observe the effects of p38 MAPK endogenous inhibition on cerebral IRI, p38 heterozygous knockdown (p38KI/+) mice were used. We hypothesized that p38 signaling might be involved in I/R injury and neurological damage reduction and that neurological behavioral deficits improve when p38 MAPK is inhibited. First, we examined the neurological damage and neurological behavioral deficit effects of I/R injury in WT mice. Cerebral I/R injury was induced by the bilateral common carotid artery occlusion (BCCAO) method. The cerebral infarction area and volume were assessed and analyzed by 2,3,5-triphenyltetrazolium chloride (TTC) staining. p38 MAPK and caspase-3 were detected by western blotting. Neuronal apoptosis was measured using TUNEL staining. Neurological deficits were detected by behavioral testing. Furthermore, to assess whether these neuroprotective effects occurred when p38 MAPK was inhibited, p38 heterozygous knockdown (p38KI/+) mice were used. We found that p38 MAPK endogenous inhibition rescued hippocampal cell apoptosis, reduced ischemic penumbra, and improved neurological behavioral deficits. These findings showed that p38 MAPK endogenous inhibition had a neuroprotective effect on IRI and that p38 MAPK may be a potential therapeutic target for cerebral IRI.

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p38 MAPK内源性抑制改善全脑缺血/再灌注小鼠的神经功能缺损。
脑缺血再灌注损伤是一个复杂的病理生理过程,可导致神经功能损伤和脑梗死的形成。p38 MAPK通路在脑I/R损伤(IRI)中引起了广泛的关注,但关于其在体内的直接作用的研究很少。本研究以p38杂合敲低(p38KI/+)小鼠为实验对象,观察p38 MAPK内源性抑制对脑IRI的影响。我们假设p38信号可能参与I/R损伤和神经损伤减轻,当p38 MAPK被抑制时,神经行为缺陷得到改善。首先,我们研究了I/R损伤对WT小鼠的神经损伤和神经行为缺陷的影响。采用双侧颈总动脉闭塞法(BCCAO)诱导脑I/R损伤。采用2,3,5-三苯基四唑氯(TTC)染色法评估脑梗死面积和脑梗死体积。western blotting检测p38 MAPK和caspase-3。TUNEL染色检测神经元凋亡。通过行为测试检测神经功能缺损。此外,为了评估当p38 MAPK被抑制时是否会发生这些神经保护作用,我们使用了p38杂合敲低(p38KI/+)小鼠。我们发现p38 MAPK内源性抑制挽救了海马细胞凋亡,减少了缺血半暗区,改善了神经行为缺陷。这些发现表明p38 MAPK内源性抑制对IRI具有神经保护作用,p38 MAPK可能是脑IRI的潜在治疗靶点。
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来源期刊
Neural Plasticity
Neural Plasticity Neuroscience-Neurology
CiteScore
5.70
自引率
0.00%
发文量
0
审稿时长
1 months
期刊介绍: Neural Plasticity is an international, interdisciplinary journal dedicated to the publication of articles related to all aspects of neural plasticity, with special emphasis on its functional significance as reflected in behavior and in psychopathology. Neural Plasticity publishes research and review articles from the entire range of relevant disciplines, including basic neuroscience, behavioral neuroscience, cognitive neuroscience, biological psychology, and biological psychiatry.
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