摘要
目的:研究依达拉奉对持续酒精摄入模型小鼠前额叶氧化水平及NRF2/HO-1通路的调节作用。方法:实验分为3组:对照组、酒精组、依达拉奉组;实验采用腹腔注射法构建持续酒精摄入小鼠模型;选用依达拉奉对模型小鼠进行干预;化学法检测模型小鼠前额叶MDA和SOD水平;实时荧光定量PCR检测NRF2/HO-1通路及其下游HMGB1通路及炎性因子mRNA表达。结果:依达拉奉干预后,与酒精组相比较,依达拉奉组小鼠前额叶MDA水平降低,SOD水平升高;NRF2及HO-1 mRNA表达水平升高(P<0.05);炎性通路及因子HMGB1、TLR4、IL-1β和TNFαmRNA表达水平降低,差异均有统计学意义(P<0.05)。结论:依达拉奉能够降低持续酒精摄入小鼠前额叶氧化水平,促进NRF2/HO-1通路基因表达,抑制炎性通路HMGB1/TLR4基因及炎性因子IL-1β和TNFαmRNA表达,发挥抗氧化及神经保护作用。
Objective:To investigate the regulatory effects of Edaravone on oxidative stress levels and the NRF2/HO-1 pathway in the prefrontal cortex of mice subjected to chronic alcohol consumption.Methods:The experiment was divided into three groups:control group,alcohol group and Edaravone group.The chronic alcohol consumption mouse model was established via intraperitoneal injection.Edaravone was administered to intervene in the model mice.Chemical methods were used to measure MDA and SOD levels in the prefrontal cortex of the model mice.Real-time quantitative PCR was used to detect the expression of mRNA in the NRF2/HO-1 pathway and its downstream HMGB1 pathway,as well as inflammatory factors(P<0.05).Results:After Edaravone intervention,compared with alcohol group,Edaravone group showed decreased MDA levels and increased SOD levels in the prefrontal cortex(P<0.05).The mRNA expression levels of NRF2 and HO-1 were elevated,while the expression levels of HMGB1,TLR4,IL-1βand TNFαmRNA in the inflammatory pathways were significantly reduced(P<0.05).Conclusion:Edaravone can reduce oxidative stress levels in the prefrontal cortex of mice with chronic alcohol consumption,promotes the expression of NRF2/HO-1 pathway genes,inhibits the HMGB1/TLR4 inflammatory pathway and the expression of inflammatory cytokines IL-1βand TNFα,thereby exerting antioxidant and neuroprotective effects.
作者
孙光涛
郑一帆
程瑜
金玉玲
戚询中
SUN Guangtao;ZHENG Yifan;CHENG Yu;JIN Yuling;QI Xunzhong(Department of Neurology,The First Affiliated Hospital of Jiamusi University,Jiamusi 154003,China)
出处
《黑龙江医药科学》
2025年第7期26-29,共4页
Heilongjiang Medicine and Pharmacy
基金
黑龙江省卫生健康委科研课题,编号:20210303090025。
