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.

中文翻译：

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右美托咪定改善体外循环大鼠术后神经认知障碍

 抽象的

 目的

探讨右美托咪定能否改善大鼠体外循环术后神经认知功能。

 方法

45只雄性SD大鼠随机分为假手术组、对照组和右美托咪定（Dex）组。 Sham组大鼠接受皮肤切除和血管结扎治疗，对照组大鼠接受体外循环（CPB）治疗，Dex组大鼠接受CPB和Dex治疗。采用Morris水迷宫试验和旷场试验评价大鼠的认知能力。检测大鼠中枢和外周区炎症介质、海马和前额叶皮层Aβ、Tau的表达以及脑组织细胞凋亡。

 结果

CPB模型大鼠认知功能明显下降，前额皮质和海马DG中caspase-3和Bax表达增加，细胞凋亡增加和小胶质细胞活化，血浆TNF-α、IL-6和TNF水平升高-α。右美托咪定减少大鼠前额皮质和海马 DG 区细胞凋亡,降低 caspase-3、bax 表达,抑制大鼠前额皮质和海马 DG 区小胶质细胞活化,降低血浆 IL-β、IL- 6、TNF-α。

 结论

右美托咪定通过抑制前额皮质和海马 DG 区域的炎症、细胞凋亡和小胶质细胞激活来发挥神经保护作用，并减轻对照组中发现的认知缺陷。