葡萄糖胺增加 O-GlcNAcylation 对成年斑马鱼视神经脑损伤模型的神经保护作用

IF 3.2 3区 医学 Q2 CLINICAL NEUROLOGY
Hyun Jae Sung, Dong Yeol Kim, Ngan An Bui, Inn-Oc Han
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引用次数: 0

摘要

本研究调查了针刺诱发成年斑马鱼视神经节损伤后端脑的行为和分子变化。在损伤后 3 天(dpi),脑组织结构明显受损,端脑神经元增殖减少,这种情况一直持续到损伤后 30 天。在损伤后 3 dpi 观察到的神经行为缺陷包括探索和社交活动减少以及学习和记忆(L/M)功能受损;所有这些缺陷在损伤后 7 dpi 全部消失。损伤导致端脑磷酸化的 cAMP 反应元件结合蛋白和 O-GlcNAcylation 减少,这两种情况在 30 dpi 时都得到了恢复。3 dpi时,GFAP表达和NF-κB p65核转位增加,30 dpi时仍未恢复。损伤在 3 dpi 时导致 O-GlcNAc 转移酶水平降低和 O-GlcNA 酶水平升高,到 30 dpi 时恢复正常。葡萄糖胺(GlcN)治疗可在 3 dpi 时显著恢复 O-GlcNAc酰化水平和 L/M 功能,还能减少 GFAP 的激活。葡萄糖处理可在 7 dpi 前恢复 L/M 功能,但用 6-重氮-5-氧代-L-正亮氨酸抑制己糖胺生物合成途径会阻止这种恢复。这些研究结果表明,O-GlcNAc 途径是解决斑马鱼脑外伤后 L/M 功能损伤的潜在治疗靶点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Neuro-protective effects of increased O-GlcNAcylation by glucosamine in an optic tectum traumatic brain injury model of adult zebrafish.

This study investigated the behavioral and molecular changes in the telencephalon following needle stab-induced injury in the optic tectum of adult zebrafish. At 3 days post-injury (dpi), there was noticeable structural damage to brain tissue and reduced neuronal proliferation in the telencephalon that persisted until 30 dpi. Neurobehavioral deficits observed at 3 dpi included decreased exploratory and social activities and impaired learning and memory (L/M) functions; all of these resolved by 7 dpi. The injury led to a reduction in telencephalic phosphorylated cAMP response element-binding protein and O-GlcNAcylation, both of which were restored by 30 dpi. There was an increase in GFAP expression and nuclear translocation of NF-κB p65 at 3 dpi, which were not restored by 30 dpi. The injury caused decreased O-GlcNAc transferase and increased O-GlcNAcase levels at 3 dpi, normalizing by 30 dpi. Glucosamine (GlcN) treatment at 3 dpi significantly restored O-GlcNAcylation levels and L/M function, also reducing GFAP activation. Glucose treatment recovered L/M function by 7 dpi, but inhibition of the hexosamine biosynthetic pathway by 6-diazo-5-oxo-L-norleucine blocked this recovery. These findings suggest that the O-GlcNAc pathway is a potential therapeutic target for addressing L/M impairment following traumatic brain injury in zebrafish.

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来源期刊
CiteScore
5.40
自引率
6.20%
发文量
118
审稿时长
6-12 weeks
期刊介绍: Journal of Neuropathology & Experimental Neurology is the official journal of the American Association of Neuropathologists, Inc. (AANP). The journal publishes peer-reviewed studies on neuropathology and experimental neuroscience, book reviews, letters, and Association news, covering a broad spectrum of fields in basic neuroscience with an emphasis on human neurological diseases. It is written by and for neuropathologists, neurologists, neurosurgeons, pathologists, psychiatrists, and basic neuroscientists from around the world. Publication has been continuous since 1942.
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