ABSTRACT

Objective

To investigate the protective effect of dexmedetomidine (Dex) on traumatic spinal cord injury (TSCI) and to evaluate the involvement of inhibition of endoplasmic reticulum (ER) stress response in the potential mechanism.

Method

Sprague–Dawley rats were randomly divided into five groups. The hind limb locomotor function of rats was evaluated at 1, 3 and 7 days after the operation. At 7 days after the operation, spinal cord specimens were obtained for hematoxylin and eosin (H&E), Nissl and TUNEL staining, as well as immunofluorescence and Western blot analyses to detect the level of apoptosis and the levels of proteins related to ER stress.

Results

7 days after the operation, Dex treatment promoted the recovery and also inhibited apoptosis of neurons in the spinal cord. Additionally, Dexinhibited the expression of proteins related to ER stress response after spinal cord injury.

Conclusions

Dex improves the neurological function of rats with TSCI and reduces apoptosis of spinal cord neurons. The potential mechanism is related to the inhibition of the ER stress response.

中文翻译：

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右美托咪定通过抑制内质网应激诱导的细胞凋亡减轻大鼠创伤性脊髓损伤

摘要

客观的

探讨右美托咪定（Dex）对创伤性脊髓损伤（TSCI）的保护作用，并评估抑制内质网（ER）应激反应的潜在机制。

方法

Sprague-Dawley 大鼠被随机分为五组。分别于术后1、3、7天评价大鼠后肢运动功能。术后第7天取脊髓标本进行苏木精和伊红(H&E)、Nissl和TUNEL染色，以及免疫荧光和Western blot分析检测细胞凋亡水平和内质网应激相关蛋白水平。

结果

术后7天，Dex治疗促进了脊髓神经元的恢复，同时也抑制了脊髓神经元的凋亡。此外，Dexin 抑制脊髓损伤后与 ER 应激反应相关的蛋白质的表达。

结论

Dex 可改善 TSCI 大鼠的神经功能并减少脊髓神经元的凋亡。潜在机制与抑制内质网应激反应有关。