Mechanism of dexmedetomidine in brain injury of infant rats via the IRE1α/NF-κB/CHOP pathway.

IF 3 4区医学 Q2 PSYCHIATRY World Journal of Biological Psychiatry Pub Date : 2025-02-01 Epub Date: 2025-01-15 DOI:10.1080/15622975.2024.2446817

Zhi Wang, Lina Zhang, Ting Wu, Xu Pan, Le Li, Xin Yang, Miao Zhang, Ying Liu

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Abstract

Objective: We investigated the mechanism of Dexmedetomidine (Dex) in infant rats with brain injury.

Methods: The infant rats underwent brain injury modelling. The motor function, spatial learning and memory abilities in rats, and the hippocampal CA1 region Nissl body level and apoptosis were evaluated by behavioural tests and histological stainings. Levels of the hippocampal CA1 region p-IRE1α, nuclear/cytoplasmic p65, CHOP, Bax and Bcl-2 proteins were determined by Western blot.

Results: Propofol anaesthesia caused brain injury in infant rats. Dex increased the hippocampal CA1 region Nissl body level, abated cell apoptosis, reduced p-IRE1α, ATF6, p-PERK/PERK and CHOP levels, decreased the Bax protein level, elevated the Bcl-2 protein level, and alleviated brain injury in infant rats. After ERS induction and the NF-κB pathway inhibition, the hippocampal CA1 region nuclear/cytoplasmic p65 ratio, CHOP level, and apoptosis were reduced in infant rats with brain injury treated with Dex, while the learning and memory abilities of rats were enhanced.

Conclusion: Dex reduced the hippocampal CA1 region cell apoptosis and enhanced learning and memory abilities by inhibiting the ERS-mediated IRE1α/NF-κB/CHOP pathway, thereby alleviating brain injury in infant rats.

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右美托咪定通过IRE1α/NF-κB/CHOP通路对幼龄大鼠脑损伤的影响机制

目的：探讨右美托咪定对幼龄脑损伤大鼠的作用机制。方法：采用大鼠脑损伤模型。通过行为学试验和组织学染色观察大鼠的运动功能、空间学习记忆能力和海马CA1区Nissl体水平及细胞凋亡。Western blot检测海马CA1区p-IRE1α、核/胞质p65、CHOP、Bax、Bcl-2蛋白水平。结果：异丙酚麻醉引起幼鼠脑损伤。Dex可提高幼鼠海马CA1区Nissl体水平，减轻细胞凋亡，降低p-IRE1α、ATF6、p-PERK/PERK和CHOP水平，降低Bax蛋白水平，升高Bcl-2蛋白水平，减轻脑损伤。右美托明对脑损伤幼鼠经ERS诱导和NF-κB通路抑制后，海马CA1区核/胞质p65比值、CHOP水平和凋亡减少，学习记忆能力增强。结论：Dex通过抑制ers介导的IRE1α/NF-κB/CHOP通路，减少海马CA1区细胞凋亡，增强学习记忆能力，从而减轻幼鼠脑损伤。

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索莱宝

sodium citrate buffer

来源期刊

World Journal of Biological Psychiatry 医学-精神病学

CiteScore

7.00

自引率

3.20%

发文量

审稿时长

6-12 weeks

期刊介绍： The aim of The World Journal of Biological Psychiatry is to increase the worldwide communication of knowledge in clinical and basic research on biological psychiatry. Its target audience is thus clinical psychiatrists, educators, scientists and students interested in biological psychiatry. The composition of The World Journal of Biological Psychiatry , with its diverse categories that allow communication of a great variety of information, ensures that it is of interest to a wide range of readers. The World Journal of Biological Psychiatry is a major clinically oriented journal on biological psychiatry. The opportunity to educate (through critical review papers, treatment guidelines and consensus reports), publish original work and observations (original papers and brief reports) and to express personal opinions (Letters to the Editor) makes The World Journal of Biological Psychiatry an extremely important medium in the field of biological psychiatry all over the world.