Mechanisms of dexmedetomidine-induced cerebral protection following ischemic brain injury via the brain-derived neurotrophic factor-tyrosine kinase receptor B pathway.

IF 1.7 4区医学 Q4 NEUROSCIENCES

Neuroreport Pub Date : 2026-05-13 Epub Date: 2026-04-28 DOI:10.1097/WNR.0000000000002256

Alimujiang Simayi, Li Qu, Xiao-Li Wang, Wan-Ying Cao, Xuan Zhao, Gui-Ping Xu

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引用次数: 0

Abstract

Objective: To investigate the protective effects of dexmedetomidine on cerebral ischemia-reperfusion injury through the activation of the brain-derived neurotrophic factor (BDNF)/tyrosine kinase receptor B (TrkB) signaling pathway.

Methods: This study utilized hippocampal neuronal oxygen-glucose deprivation/reoxygenation (OGD/R) models and rat middle cerebral artery occlusion models, with dexmedetomidine intervention.

Results: Compared with the sham-operated group, the model group rats exhibited a significant increase in Zea-Longa scores, a marked prolongation of the escape latency, a notable reduction in the number of platform crossings, a significant increase in the percentage of cerebral infarct size, and a marked decrease in the expression of BDNF, TrkB, and Bcl-2 proteins and mRNA ( P < 0.05). The dexmedetomidine group showed significantly better outcomes in all above parameters compared to the model group. Compared with the control group, the OGD/R group exhibited a reduction in hippocampal neuronal cell viability, a significant increase in apoptosis rate, elevated expression of Bax and C-caspase-3 proteins, a marked decrease in Bcl-2 protein levels, and a significant reduction in the expression of BDNF and TrkB proteins and mRNA ( P < 0.05).

Conclusion: Dexmedetomidine exerts significant neuroprotective effects by activating the BDNF/TrkB signaling pathway, thereby alleviating ischemic brain injury.

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右美托咪定通过脑源性神经营养因子-酪氨酸激酶受体B通路诱导缺血性脑损伤脑保护机制

目的：探讨右美托咪定通过激活脑源性神经营养因子(BDNF)/酪氨酸激酶受体B （TrkB）信号通路对脑缺血再灌注损伤的保护作用。方法：采用海马神经元氧葡萄糖剥夺/再氧合（OGD/R）模型和大鼠大脑中动脉闭塞模型，右美托咪定干预。结果：与假手术组比较，模型组大鼠Zea-Longa评分明显升高，逃避潜伏期明显延长，穿越平台次数明显减少，脑梗死面积百分比明显增加，BDNF、TrkB、Bcl-2蛋白及mRNA表达明显降低(P)。右美托咪定通过激活BDNF/TrkB信号通路发挥显著的神经保护作用，从而减轻缺血性脑损伤。

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

Neuroreport 医学-神经科学

CiteScore

3.20

自引率

0.00%

发文量

150

审稿时长

1 months

期刊介绍： NeuroReport is a channel for rapid communication of new findings in neuroscience. It is a forum for the publication of short but complete reports of important studies that require very fast publication. Papers are accepted on the basis of the novelty of their finding, on their significance for neuroscience and on a clear need for rapid publication. Preliminary communications are not suitable for the Journal. Submitted articles undergo a preliminary review by the editor. Some articles may be returned to authors without further consideration. Those being considered for publication will undergo further assessment and peer-review by the editors and those invited to do so from a reviewer pool. The core interest of the Journal is on studies that cast light on how the brain (and the whole of the nervous system) works. We aim to give authors a decision on their submission within 2-5 weeks, and all accepted articles appear in the next issue to press.