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机构地区:[1]广东省东莞市常平医院手足外科,广东东莞523573
出 处:《海南医学院学报》2017年第5期577-580,共4页Journal of Hainan Medical University
基 金:东莞市医疗卫生项目(200510515035114)~~
摘 要:目的:研究抑制P38MAPK对皮瓣缺血再灌注损伤过程中炎症因子、细胞凋亡的影响。方法:选择Wistar大鼠作为实验动物,随机分为对照组、模型组、干预组,对照组常规制作腹壁浅动静脉皮瓣,模型组制作缺血再灌注皮瓣模型,干预组制作缺血再灌注皮瓣模型并给予SB202190干预。皮瓣制作后8d时收集组织,测定炎症因子、凋亡分子的表达量以及氧化应激指标的含量。结果:模型组大鼠皮瓣组织中NF-κB、IL-6、TNF-α、Bax、Caspase-3的mRNA表达量以及蛋白表达量均显著高于对照组,ROS、MDA、AOPP、8-OHdG的含量均显著高于对照组,Bcl-2的mRNA表达量以及蛋白表达量均显著低于对照组;干预组大鼠皮瓣组织中NF-κB、IL-6、IL-8、TNF-α、Bax、Caspase-3的mRNA表达量以及蛋白表达量均显著低于模型组,ROS、MDA、AOPP、8-OHdG的含量均显著低于模型组,Bcl-2的mRNA表达量以及蛋白表达量均显著高于模型组。结论:抑制P38MAPK能够减轻炎症反应、氧化应激反应以及细胞凋亡所造成的移植皮瓣缺血再灌注损伤。Objective:To study the effect of inhibiting P38 MAPK on inflammatory factors and cell apoptosis during flap ischemia-reperfusion injury.Methods:Wistar rats were selected as experimental animals and randomly divided into control group,model group and intervention group,control group were made into routine abdominal superficial arteriovenous flap models,model group were made into ischemia-reperfusion flap models and intervention group were made into ischemia-reperfusion flap models and then received SB202190 intervention.Eight days after flap making,tissue was collected to detect the expression of inflammatory factors and apoptosis molecules as well as the levels of oxidative stress indicators.Results:NF-κB,IL-6,TNF-α,Bax and Caspase-3 mRNA expression and protein expression in flap tissue of model group were significantly higher than those of control group,ROS,MDA,AOPP and 8-OHdG levels were significantly higher than those of control group,and Bcl-2mRNA expression and protein expression were significantly lower than those of control group;NF-κB,IL-6,TNF-α,Bax and Caspase-3mRNA expression and protein expression in flap tissue of intervention group were significantly lower than those of model group,ROS,MDA,AOPP and 8-OHdG levels were significantly lower than those of model group,and Bcl-2mRNA expression and protein expression were significantly higher than those of model group.Conclusion:Inhibiting P38 MAPK can reduce the transplanted flap ischemia-reperfusion injury caused by inflammation,oxidative stress and cell apoptosis.
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