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右美托咪定立体定向注射减轻双侧颈总动脉闭塞后神经元丢失:BDNF 表达的上调。

Dexmedetomidine Stereotaxic Injection Alleviates Neuronal Loss Following Bilateral Common Carotid Artery Occlusion Up-Regulation of BDNF Expression.

机构信息

Department of Anesthesiology and Pain Medicine, Chosun University Hospital, Gwang-ju, Republic of Korea.

Department of Neurosurgery, Chosun University Hospital, Gwang-ju, Republic of Korea.

出版信息

In Vivo. 2024 Jan-Feb;38(1):184-189. doi: 10.21873/invivo.13424.

DOI:10.21873/invivo.13424
PMID:38148065
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10756478/
Abstract

BACKGROUND/AIM: Neurogenesis is an important process in the recovery from neurological damage caused by ischemic lesions. Endogenous neurogenesis is insufficient to restore neuronal damage following cerebral ischemia. Dexmedetomidine (DEX) exerts neuroprotective effects against cerebral ischemia and ischemia/reperfusion injury. DEX promotes neurogenesis, including neuronal proliferation and maturation in the hippocampus. In a previous study, we showed that early neurogenesis increased 3 days after bilateral common carotid artery occlusion (BCCAO). In this study, we investigated the effect of DEX on neurogenesis 3 days after BCCAO.

MATERIALS AND METHODS

Male Sprague-Dawley (SD) rats (7-8 weeks old) were used as a BCCAO model. Right and left common carotid arteries of the rats were occluded using 4-0 silk sutures. Two hours after surgery, an intracranial DEX injection was administered to rats that underwent surgery using a stereotaxic injector. Brains were obtained from control and BCCAO rats 3 days after surgery. Immunohistochemistry was performed on the cortex and dentate gyrus of the hippocampus using a NeuN antibody. Western blot was performed with HIF1α and brain-derived neurotrophic factor (BDNF) antibodies.

RESULTS

The number of mature neurons decreased 3 days after BCCAO, but DEX treatment alleviated neural loss in the parietal cortex and hippocampus. Up-regulation of BDNF was also observed after dexmedetomidine treatment.

CONCLUSION

Stereotaxic injection of dexmedetomidine alleviates neural loss following BCCAO by up-regulating BDNF expression.

摘要

背景/目的:神经发生是由缺血性病变引起的神经损伤恢复的重要过程。内源性神经发生不足以恢复脑缺血后的神经元损伤。右美托咪定(DEX)对脑缺血和缺血/再灌注损伤具有神经保护作用。DEX 促进神经发生,包括海马中的神经元增殖和成熟。在之前的研究中,我们表明双侧颈总动脉闭塞(BCCAO)后 3 天早期神经发生增加。在这项研究中,我们研究了 DEX 对 BCCAO 后 3 天神经发生的影响。

材料和方法

雄性 Sprague-Dawley(SD)大鼠(7-8 周龄)用作 BCCAO 模型。使用 4-0 丝线结扎大鼠的右颈总动脉和左颈总动脉。手术后 2 小时,使用立体定向注射器对接受手术的大鼠进行颅内 DEX 注射。手术后 3 天从对照和 BCCAO 大鼠中取出大脑。使用 NeuN 抗体对大脑皮质和海马齿状回进行免疫组织化学染色。使用 HIF1α 和脑源性神经营养因子(BDNF)抗体进行 Western blot。

结果

BCCAO 后 3 天成熟神经元数量减少,但 DEX 处理减轻了顶叶皮质和海马的神经丢失。DEX 处理后还观察到 BDNF 的上调。

结论

立体定向注射右美托咪定通过上调 BDNF 表达减轻 BCCAO 后的神经丢失。

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