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。
Dexmedetomidine alleviates traumatic spinal cord injury in rats via inhibiting apoptosis induced by endoplasmic reticulum stress.
作者信息
Liu Yi-Bin, Liu Wei-Feng, Chen Wei-Can, Li Wei, Lin Yan-Ling, Xu Chong-Jun, He He-Fan
机构信息
Department of Anesthesiology, The Second Affiliated Hospital of Fujian Medical University, Quanzhou, China.
Department of ICU, Wuhan Third Hospital, Wuhan University, Wuhan, China.
出版信息
Neurol Res. 2022 Mar;44(3):275-284. doi: 10.1080/01616412.2021.1979750. Epub 2021 Sep 17.
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.
目的
探讨右美托咪定（Dex）对创伤性脊髓损伤（TSCI）的保护作用，并评估内质网（ER）应激反应抑制在其潜在机制中的作用。
方法
将Sprague-Dawley大鼠随机分为五组。在术后1、3和7天评估大鼠后肢运动功能。术后7天，获取脊髓标本进行苏木精-伊红（H&E）、尼氏和TUNEL染色，以及免疫荧光和蛋白质印迹分析，以检测凋亡水平和与ER应激相关的蛋白质水平。
结果
术后7天，Dex治疗促进了脊髓神经元的恢复并抑制了其凋亡。此外，Dex抑制了脊髓损伤后与ER应激反应相关的蛋白质表达。
结论
Dex改善了TSCI大鼠的神经功能并减少了脊髓神经元的凋亡。其潜在机制与抑制ER应激反应有关。
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