Glycine Receptor Beta Subunit (GlyR-β) Promotes Potential Angiogenesis and Neurological Regeneration during Early-Stage Recovery after Cerebral Ischemia Stroke/Reperfusion in Mice.

IF 2.5 4区医学 Q3 NEUROSCIENCES

Journal of integrative neuroscience Pub Date : 2024-08-15 DOI:10.31083/j.jin2308145

Yuan Xu, Yushi Yang, Jie Yang, Junshuan Cui, Jian Yan, Jiannan Jiang, Zhangwei Yan, Hua Yang

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引用次数: 0

Abstract

Background: Ischemic stroke is mainly caused by cerebral artery thrombosis. This study investigated the role of glycine receptor beta subunit (GlyR-β) in the recovery from cerebral ischemia stroke/reperfusion.

Methods: The oxygen glucose deprivation and recovery (OGD/R) bEnd3 cell model and the middle cerebral artery occlusion/reperfusion (MCAO/R) mouse model were used in this study.

Results: Expression of both the GlyR-β gene and vascular endothelial growth factor (Vegf), cell proliferation, and tube formation ability was decreased in bEnd3 cells after OGD/R, and was reversed by overexpression of GlyR-β. Neurological function, asindicated by Zea Longa scores, area of cerebral ischemia, and pathological changes were increased in mice after MCAO/R, and were ameliorated by overexpression of the glycine receptor beta (Glrb) gene at 24 h and 7 d after MCAO/R. Expression of GlyR-β and Gap-43 was decreased, and the expression of CD34, Vegf, and Bdnf, and cell growth as determined by a bromodeoxyuridine (BrdU) assay, increased in the affected brain tissue of MCAO/R mice in a time-dependent manner. GlyR-β overexpression resulted in enhanced expression of CD34, Vegf, Growth association protein 43 (Gap-43), and brain-derived neurotrophic factor (Bdnf) and cell growth in affected brain tissue of MCAO/R mice in a time-dependent manner.

Conclusions: GlyR-β promoted potential angiogenesis and neurological regeneration in affected brain tissue, thus promoting recovery from cerebral ischemia stroke/reperfusion.

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甘氨酸受体β亚基（GlyR-β）促进小鼠脑缺血中风/再灌注后早期恢复过程中的潜在血管生成和神经再生。

背景：缺血性脑卒中主要由脑动脉血栓形成引起。本研究探讨了甘氨酸受体β亚基（GlyR-β）在脑缺血卒中/再灌注恢复中的作用：方法：本研究采用氧葡萄糖剥夺和恢复（OGD/R）bEnd3细胞模型和大脑中动脉闭塞/再灌注（MCAO/R）小鼠模型：结果：OGD/R后，bEnd3细胞中GlyR-β基因和血管内皮生长因子（Vegf）的表达、细胞增殖和管形成能力均下降，而过表达GlyR-β可逆转这种下降。MCAO/R后小鼠的神经功能，如Zea Longa评分、脑缺血面积和病理变化均有所增加，而在MCAO/R后24 h和7 d过表达甘氨酸受体β（Glrb）基因后，情况有所改善。在MCAO/R小鼠受影响的脑组织中，GlyR-β和Gap-43的表达量减少，CD34、Vegf和Bdnf的表达量增加，溴脱氧尿苷（BrdU）测定的细胞生长量增加，且呈时间依赖性。GlyR-β过表达导致CD34、Vegf、生长联合蛋白43（Gap-43）和脑源性神经营养因子（Bdnf）表达增强，MCAO/R小鼠受影响脑组织中的细胞生长呈时间依赖性：结论：GlyR-β能促进受累脑组织的潜在血管生成和神经再生，从而促进脑缺血卒中/再灌注后的恢复。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Journal of integrative neuroscience 医学-神经科学

CiteScore

2.80

自引率

5.60%

发文量

173

审稿时长

2 months

期刊介绍： JIN is an international peer-reviewed, open access journal. JIN publishes leading-edge research at the interface of theoretical and experimental neuroscience, focusing across hierarchical levels of brain organization to better understand how diverse functions are integrated. We encourage submissions from scientists of all specialties that relate to brain functioning.