Nuclear factor erythroid 2-related factor 2 antibody attenuates thermal hyperalgesia in the dorsal root ganglion: Neurochemical changes and behavioral studies after sciatic nerve-pinch injury
Nuclear factor erythroid 2-related factor 2 antibody attenuates thermal hyperalgesia in the dorsal root ganglion: Neurochemical changes and behavioral studies after sciatic nerve-pinch injury
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核因子红细胞 2 相关因子 2 抗体减弱背根神经节的热痛觉过敏：坐骨神经挤压损伤后的神经化学变化和行为研究
DOI：
10.1016/j.injury.2016.06.006
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发表时间：
2016
影响因子：
2.5
通讯作者：
Li Xian Hui
中科院分区：
文献类型：
--
作者：
Xiang Qiong;Yu Chao;Zhu Yao Feng;Li Chun Yan;Tian Rong Bo;Li Xian Hui
氧化应激在几种周围神经损伤模型中产生，核因子红系相关因子2(NRF2)被激活以发挥抗氧化作用。神经损伤后，还会进行剧烈疼痛的行为。然而，关于Nrf2在这一痛苦过程中的作用的研究很少。因此，在本研究中，我们比较了坐骨神经夹伤后应用Nrf2抗体对幼年小鼠疼痛行为和背根神经节神经元神经化学变化的影响。在夹断神经损伤后，我们发现应用Nrf2抗体(5ul，1 mg/ml)后，这种损伤动物的热痛程度明显减轻，抗Nrf2治疗的损伤组背根神经节神经元的磷酸化ERK(p-ERK)和凋亡蛋白(Bcl6)也比生理盐水组下调。综上所述，上述结果提示，Nrf2抗体通过ERK途径减少热痛觉过敏，下调细胞凋亡途径中的Bcl6蛋白可能对抗Nrf2作用引起的蛋白缺失具有保护作用，并提示Nrf2抑制剂治疗神经损伤的新策略。
Oxidative stress is generated in several peripheral nerve injury models.Nuclear factor erythroid 2-related factor 2 (Nrf2) is activated to have a role in antioxidant effect. After nerve injury, the severely painful behavior is also performed. However, little has been explored regarding the function of Nrf2 in this painful process. Therefore, in this study, we compared the effects of Nrf2 antibody administration following sciatic nerve-pinch injury on painful behavior induced in young mice and neurochemical changes in dorsal root ganglion neurons. After pinch nerve injury, we found that the magnitude of the thermal allodynia was significantly decreased after application of Nrf2 antibody (5ul, 1 mg/ml) in such injured animals and phosphorylated ERK(p-ERK) as well as the apoptotic protein (i.e., Bcl-6) in DRG neurons were also down-regulated in the anti-Nrf2-treated injured groups compared to the saline-treated groups. Taken collectively, these data suggested that the Nrf2 antibody reduced thermal hyperalgesia via ERK pathway and the down regulation of Bcl-6 protein from the apoptosis pathway might be protecting against the protein deletions caused by anti-Nrf2 effect and suggested the new therapeutic strategy with Nrf2 inhibitor following nerve injury.