右美托咪定激活Nrf2/HO-1信号通路抑制氧化应激缓解大鼠神经病理性疼痛  

Dexmedetomidine activates the Nrf2/HO-1 signaling pathway to inhibit oxidative stress to relieve neuropathic pain in rats

作　　者：于东海[1] 张振 赵博[1] 周南 YU Dong-hai;ZHANG Zhen;ZHAO Bo;ZHOU Nan(Department of Anesthesiology,Dalian Central Hospital,Dalian 116033;Department of Anesthesiology,General Hospital of the Northern Theater Command,Shenyang 110016,China)

机构地区：[1]大连市中心医院麻醉科,辽宁大连116033 [2]北部战区总医院麻醉科,辽宁沈阳110016

出　　处：《解剖科学进展》2021年第2期169-173,共5页Progress of Anatomical Sciences

基　　金：辽宁省自然科学基金(20180551091)。

摘　　要：目的探讨右美托咪定(dexmedetomidine, DEX)对神经性疼痛大鼠坐骨神经处神经阻滞作用及可能的机制。方法将SD大鼠随机分为假手术组(Sham)、慢性坐骨神经结扎建立神经病理性疼痛模型组(CCI)和DEX治疗组(DEX);测定各组大鼠机械性缩足反射阈值和热缩爪潜伏期;HE染色观测各组大鼠坐骨神经病理改变;试剂盒检测大鼠坐骨神经中超过氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)活性及丙二醛(MDA)含量;TUNEL检测坐骨神经处细胞凋亡;Western blot检测Nrf2及HO-1蛋白的表达。结果与CCI组相比,DEX提高CCI大鼠的机械痛阈值和热缩爪潜伏期,改善CCI大鼠坐骨神经病理损伤,显著增加坐骨神经中SOD、GSH-Px活性,降低MDA含量并减少神经细胞的凋亡,显著增加坐骨神经中Nrf2及HO-1蛋白表达水平(P<0.05)。结论 DEX缓解CCI诱导的神经病理性疼痛,改善坐骨神经损伤,与激活Nrf2/HO-1信号通路抑制氧化应激相关。Objective To investigate the effect of dexmedetomidine(DEX) on the nerve block of sciatic nerve in rats with neuropathic pain and its possible mechanism. Methods SD rats were randomly divided into sham operation group(Sham), model group(chronic sciatic nerve ligation, CCI) and DEX treatment group(DEX). The threshold of mechanical foot retraction reflex and latent period of thermal claw were measured, the changes of sciatic neuropathy were observed by HE staining;The activities of superoxide dismutase(SOD) and glutathione peroxidase(GSH-Px), and the content of malondialdehyde(MDA) in the sciatic nerve were detected by kits, the number of apoptotic cells in sciatic nerve was detected by TUNEL, the expressions of Nrf2 and HO-1 were detected by Western blot. Results DEX increased the mechanical pain threshold and heat shrinking paw latency of CCI rats, improved the pathological injury of sciatic nerve significantly, increased the activity of SOD and GSH-Px in sciatic nerve, reduced the content of MDA and inhibited the apoptosis of nerve cells, and also increased the expression level of Nrf2 and HO-1 proteins in sciatic nerve(P<0.05). Conclusion DEX relieved CCI-induced neuropathic pain and improved sciatic nerve injury, which is related to the activation of Nrf2/HO-1 signaling pathway to inhibit oxidative stress.

关 键 词：右美托咪定 神经病理性疼痛 坐骨神经阻滞 氧化应激 Nrf2/HO-1信号通路 大鼠 

分 类 号：R593.22[医药卫生—内科学]