Nrf2/ARE信号通路激活对偏头痛大鼠神经源性炎症的影响

目的探讨核因子E2相关因子2/抗反应元件(Nrf2/ARE)通路激活对硝酸甘油(NTG)诱导的偏头痛模型大鼠神经源性炎症的影响。方法将大鼠随机分为NS组、莱菔硫烷(SFN)+NS组、NTG组、H₂O+NTG组及SFN+NTG组,6只/组。拍摄大鼠挠头视频,应用ELISA检测颈静脉血CGRP浓度,应用Western Blot检测大鼠硬脑膜Nrf2、HO1、NQO1、NF-κB、TNF-α及IL-1β的表达。结果SFN+NTG组各时间段大鼠挠头次数少于H₂O+NTG组(P<0.01)。SFN+NTG组的核Nrf2及下游HO1、NQO1蛋白的表达均高于NTG组与H₂O+NTG组,颈静脉血CGRP浓度低于H₂O+NTG组,硬脑膜NF-κB及TNF-α、IL-1β表达均低于NTG组与H₂O+NTG组(P<0.01)。结论Nrf2/ARE信号通路的激活可减少NTG诱导的偏头痛大鼠挠头次数,降低颈静脉CGRP的浓度,抑制硬脑膜炎症因子的表达,发挥神经保护作用。

Effect of Nrf2/ARE signaling pathway activation on neurogenic inflammation in migraine rats

Objective To investigate the effect of activation of nuclear factor erythroid 2 related factor 2/antioxidant response element(Nrf2/ARE)pathway on neurogenic inflammation in migraine model rats induced by nitroglycerin(NTG).Methods The rats were randomly divided into NS group,sulforaphane(SFN)+NS group,NTG group,H₂O+NTG group and SFN+NTG group,with 6 rats in each group.The video of rats scratching their heads was taken.The concentration of CGRP in jugular blood was detected by ELISA.The expression of Nrf2,HO1,NQO1,NF-κB in dura mater,TNF-αand IL-1βwere detected by Western Blot.Results The numbers of head scratching at each time period in the SFN+NTG group were less than those in the H₂O+NTG group(P<0.01).The expression of Nrf2,downstream HO1 and NQO1 protein in the SFN+NTG group were higher than those in the NTG group and the H₂O+NTG group,the concentration of CGRP in jugular blood was lower than that in the H₂O+NTG group,and the expression of NF-κB in dura mater,TNF-αand IL-1βwere lower than those in the NTG group and the H₂O+NTG group(P<0.01).Conclusion The activation of Nrf2/ARE signaling pathway can reduce the number of head scratching and the concentration of CGRP in jugular vein of NTG induced migraine rats,inhibit the expression of hard meningitis factor,and play a neuroprotective role.