Objective:To explore the effect of edaravone on the oxygen free-radical damage and inflammatory re-sponse 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 in-creased 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:Edara-vone relieves the cerebral infarction area,apoptosis,oxidative stress and inflammatory response in hypoxia-reoxygen-ation rat by inhibiting phosphorylation of NF-κB p65.%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 dUTP 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(superox-ide 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(in-terleukin-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 -1 β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.
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