鹅不食草介导Nrf2/HO-1信号通路在脑缺血再灌注中抗氧化抗炎作用机制研究

目的:探讨鹅不食草对脑缺血再灌注大鼠Nrf2/HO-1信号通路介导的氧化应激反应和神经炎症影响。方法:SD大鼠分为假手术组、脑缺血组、依达拉奉组、鹅不食草100 mg/kg剂量组、鹅不食草200 mg/kg剂量组、鹅不食草400 mg/kg剂量组。采用中动脉栓塞介导大鼠缺血损伤,连续给药后评价大鼠神经功能,脑组织脑梗死面积、氧化因子、炎症因子含量,Nrf2、HO-1 mRNA与蛋白含量。结果:与假手术组相比,脑缺血组大鼠神经功能显著损伤(P<0.05),脑梗死体积增加(P<0.05),氧化因子、炎症因子含量增加(P<0.05)。与脑缺血组相比,鹅不食草组与依达拉奉组改善了大鼠神经功能(P<0.05),减少脑梗死面积(P<0.05),抑制氧化应激与炎症反应(P<0.05),而Nrf2、HO-1 mRNA与蛋白表达增加(P<0.05)。结论:鹅不食草可以介导Nrf2/HO-1信号通路减少大鼠脑中氧化应激反应与炎症因子含量,改善大鼠神经功能。

Centipeda minima mediated anti-oxidation and anti-inflammatory through Nrf2/HO-1 pathway in cerebral ischemia-reperfusion

Objective:To explore the effects of centipeda minima on oxidative stress response and neuroinflammation through Nrf2/HO-1 signaling pathway in rats with cerebral ischemia-reperfusion.Methods:SD rats were randomly divided into sham group,cerebral hypoxia group,edaravone group,centipeda minima 100 mg/kg,200 mg/kg,400 mg/kg.The middle cerebral artery occlusion operations were applied for ischemic injury in rats.The nerve function of rats was evaluated after continuous drug administration.The brain tissue was taken for cerebral infarction detection,oxidative factors,inflammatory factors and the expression of Nrf2 mRNA,HO-1 mRNA and proteins.Results:Compared with sham group,cerebral hypoxia group had significant neurological function damage(P<0.05),increased cerebral infarction area(P<0.05),and elevated levels of oxidative factors and inflammatory factors(P<0.05).Compared with cerebral hypoxia group,centipeda minima and edaravone administration improved nerve function in rats(P<0.05),reduced cerebral infarction(P<0.05),reduced the expression of oxidative factors and inflammatory factors in the brain(P<0.05),increased the expression of Nrf2,HO-1 mRNA and protein(P<0.05).Conclusion:Centipeda minima can improve the nerve function through Nrf2,HO-1 signaling pathway which mediate oxidative stress and inflammation reduction in the brain of rats.