依达拉奉抑制NF-κB p65磷酸化缓解脑缺氧-复氧大鼠模型的氧自由基损伤和炎症反应  

Edaravone alleviates the oxygen free-radical damage and inflammatory response of hypoxia-reoxygenation rat by inhibiting phosphorylation of NF-κB p65

作　　者：侯立维[1] 孔丽娜 杜开先[2] Hou Liwei;Kong Lina;Du Kaixian(Department of Neurology,Second Affiliated Hospital of Zhengzhou University,Henan Zhengzhou 450014,China;Department of Neurology,Third Affiliated Hospital of Zhengzhou University,Henan Zhengzhou 450052,China)

机构地区：[1]郑州大学第二附属医院神经内科一病区,河南郑州450014 [2]郑州大学第三附属医院神经内科二病区,河南郑州450052

出　　处：《现代肿瘤医学》2018年第23期3717-3721,共5页Journal of Modern Oncology

基　　金：河南省基础与前沿技术研究计划项目(编号:142300410065)

摘　　要：目的:探讨依达拉奉对脑缺氧-复氧大鼠氧化应激损伤和炎症反应的影响。方法:大鼠随机分为3组:对照组(Ctrl)、缺氧-复氧组(H/R)和依达拉奉处理组(H/R+EV)。脱氧核糖核苷酸末端转移酶介导的缺口末端标记(terminal deoxynucleotidyl transferase-mediated d UTP nick labeling,TUNEL)染色检测细胞凋亡。ELISA检测丙二醛(malonaldehyde,MDA),乳酸脱氢酶(lactic dehydrogenase,LDH),超氧化物歧化酶(superoxide dismutase,SOD),白细胞介素(interleukin,IL)-6和IL-10水平。蛋白印迹检测细胞介素受体拮抗剂(interleukin-1 receptor antagonist,IL-1Ra),IL-1β,NF-κB p65和p-p65的蛋白水平。结果:H/R组脑梗面积大于对照组(P <0. 01)。H/R+EV组脑梗面积小于H/R组(P <0. 01)。H/R组脑组织细胞凋亡高于对照组(P <0. 01)。H/R+EV组脑组织细胞凋亡低于H/R组(P <0. 01)。与对照组相比,H/R组脑组织MDA和LDH水平上升,SOD水平降低(P <0. 01)。与H/R组相比,H/R+EV组脑组织MDA和LDH水平下降,SOD水平升高(P <0. 01)。与对照组相比,H/R组脑组织IL-6水平和IL-1 Ra/IL-1β比值上升,IL-10水平降低(P <0. 01)。与H/R组相比,H/R+EV组脑组织IL-6水平和IL-1Ra/IL-1β比值下降,IL-10水平升高(P <0. 01)。H/R组脑组织p-p65/p65比值高于对照组(P <0. 01)。H/R+EV组脑组织p-p65/p65比值低于H/R组(P <0. 01)。结论:依达拉奉抑制NF-κB p65磷酸化缓解脑缺氧-复氧大鼠脑梗面积,细胞凋亡,氧化应激及炎症反应。Objective：To explore the effect of edaravone on the oxygen free-radical damage and inflammatory response in hypoxia-oxygenated rat.Methods：Rats were divided into three groups：Control （Ctrl） group,hypoxia-reoxygenation （H/R） group and hypoxia-reoxygenation＋edaravone （H/R＋EV） group.Apoptosis was detected by terminal deoxynucleotidyl transferase-mediated dUTP nick labeling （TUNEL）.The levels of malonaldehyde （MDA）,lactic dehydrogenase （LDH）,superoxide dismutase （SOD）,interleukin （IL）-6 and IL-10 were tested by ELISA.The protein levels of interleukin-1 receptor antagonist （IL-1Ra）,IL-1β,NF-κB p65 and p-p65 were measured by Western blot.Results：The cerebral infarction area in H/R group was larger than control group （P〈0.01）.The cerebral infarction area in H/R＋EV group was smaller than H/R group （P〈0.01）.Apoptosis of brain tissue in H/R group was higher than control group （P〈0.01）.Apoptosis of brain tissue in H/R＋EV group was lower than H/R group （P〈0.01）.Compared with control group,the levels of MDA and LDH in H/R group were increased with declined levels of SOD （P〈0.01）.Compared with H/R group,the levels of MDA and LDH in H/R＋EV group were decreased with enhancive levls of SOD （P〈0.01）.Compared with control group,the levels of IL-6 and the rate of IL-1Ra/IL-1β in H/R group were elevated with reduced levels of IL-10 （P〈0.01）.Compared with H/R group,the levels of IL-6 and the rate of IL-1Ra/IL-1β in H/R＋EV group were attenuated with increased levls of IL-10 （P〈0.01）.The rate of p-p65/p65 in H/R group was higher than control group （P〈0.01）.The rate of p-p65/p65 in H/R＋EV group was lower than H/R group （P〈0.01）.Conclusion：Edaravone relieves the cerebral infarction area,apoptosis,oxidative stress and inflammatory response in hypoxia-reoxygenation rat by inhibiting phosphorylation of NF-κB p65.

关 键 词：依达拉奉 缺氧-复氧损伤 氧化应激 炎症反应 NF-ΚB p65 

分 类 号：R730.23[医药卫生—肿瘤]