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右美托咪定改善体外循环后大鼠术后神经认知障碍。

Dexmedetomidine improves postoperative neurocognitive disorder after cardiopulmonary bypass in rats.

机构信息

Department of Anesthesiology, Hospital (T.C.M)) Affiliated to Southwest Medical University, Luzhou, Sichuan, China.

出版信息

Neurol Res. 2021 Feb;43(2):164-172. doi: 10.1080/01616412.2020.1833154. Epub 2020 Oct 19.

DOI:10.1080/01616412.2020.1833154
PMID:33076786
Abstract

PURPOSE

To investigate whether dexmedetomidine can improve postoperative neurocognitive function after cardiopulmonary bypass in rats.

METHODS

A total of 45 male Sprague Dawley (SD) rats were randomly divided into sham group, control group, and dexmedetomidine (Dex) group. The rats in the sham group received skin excision and blood vessel ligation treatment, rats in the control group received cardiopulmonary bypass (CPB), and rats in the Dex group received CPB and Dex treatment. Morris water maze test and open-field tests were used to evaluate the rats' cognition. The expression of inflammatory mediators in the rats' central and peripheral regions, Aβ and Tau in the hippocampus and prefrontal cortex, and apoptosis in brain tissue were measured.

RESULTS

The CPB model rats were found to have significantly decreased cognitive function, increased expression of caspase-3 and Bax in the prefrontal cortex and hippocampus DG, increased apoptosis and activated microglia, and increased plasma levels of TNF-α, IL-6, and TNF-α. Dexmedetomidine reduced apoptosis in the prefrontal cortex and hippocampus DG region of rats, decreased the expression of caspase-3 and bax, inhibited microglia activation in the prefrontal cortex and hippocampus DG region of rats, and decreased the plasma levels of IL-β, IL-6, and TNF-α.

CONCLUSIONS

Dexmedetomidine plays a neuroprotective role by inhibiting inflammation, apoptosis, and microglia activation in the prefrontal cortex and hippocampal DG region, and attenuates the cognitive deficit identified in the control group.

摘要

目的

探讨右美托咪定是否可以改善体外循环后大鼠的术后神经认知功能。

方法

将 45 只雄性 Sprague Dawley(SD)大鼠随机分为假手术组、对照组和右美托咪定(Dex)组。假手术组大鼠接受皮肤切除和血管结扎处理,对照组大鼠接受体外循环(CPB),Dex 组大鼠接受 CPB 和 Dex 治疗。使用 Morris 水迷宫试验和旷场试验评估大鼠的认知功能。测量大鼠中枢和外周区域炎症介质的表达、海马和前额叶皮质中的 Aβ和 Tau,以及脑组织中的细胞凋亡。

结果

CPB 模型大鼠的认知功能明显下降,前额叶皮质和海马 DG 区 caspase-3 和 Bax 的表达增加,细胞凋亡和激活的小胶质细胞增加,血浆中 TNF-α、IL-6 和 TNF-α 的水平升高。右美托咪定降低了大鼠前额叶皮质和海马 DG 区的细胞凋亡,降低了 caspase-3 和 Bax 的表达,抑制了大鼠前额叶皮质和海马 DG 区小胶质细胞的激活,降低了血浆中 IL-β、IL-6 和 TNF-α 的水平。

结论

右美托咪定通过抑制前额叶皮质和海马 DG 区的炎症、细胞凋亡和小胶质细胞激活发挥神经保护作用,减轻了对照组大鼠的认知缺陷。

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