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作 者:方文慧[1] 姚咏明[1] 李红云[1] 董宁[1] 于燕[1] 陆连荣[1] 施志国[1] 盛志勇[1]
机构地区:[1]解放军第304医院创伤外科中心,北京100037
出 处:《中华实验外科杂志》2002年第2期150-151,共2页Chinese Journal of Experimental Surgery
基 金:国家重点基础研究发展规划项目(G19990 54 2 0 3) ;国家自然科学基金资助项目( 39870 2 86 );军队杰出中青年人才专项基金( 98J0 13)资助
摘 要:目的 探讨烫伤脓毒症时生物喋呤对肝组织丝裂原激活蛋白激酶 p38(p38MAPK)活化的影响及其病理生理意义。方法 采用大鼠 2 0 %TBSAⅢ度烫伤复合金黄色葡萄球菌攻击模型 ,动物随机分为正常对照组、烫伤对照组、烫伤脓毒症组和生物喋呤合成抑制剂 (DAHP)治疗组。采用Westernblot技术检测肝组织 p38MAPK的磷酸化状态。 结果 正常肝组织磷酸化 p38MAPK蛋白水平很低。烫伤脓毒症后 2h ,肝组织 p38MAPK磷酸化水平即明显升高 ,且持续至伤后 2 4h。生物喋呤合成抑制剂早期干预则可显著降低肝组织 p38MAPK磷酸化水平。结论 烫伤脓毒症时生物喋呤与肝组织 p38MAPK活化密切相关。Objective To investigate the effect of biopterin (tetrahydrobiopterin and more oxidized species) on p38 mitogen activated protein kinase (MAPK) activation in liver tissues during postburn sepsis.Methods Rats inflicted with 20% TBSA Ⅲ degree scald followed by Staphylococcus aureus sepsis were used as the experimental subjects.Animals were randomly divided into four groups:normal control group,scald control group,postburn sepsis group and 2,4 diamino 6 hydroxy pyrimidine (DAHP) treatment group.Tissue samples in liver were collected to measure levels of phosphorylation of p38 MAPK.Results Western blot analysis revealed a low basal level of phosphorylation of p38 MAPK in liver.Levels of tissue p38 MAPK phosphorylation evidently increased at 2?h after thermal injury combined with Staphylococcus aureus infection,and continued to increase afterwards.Treatment with DAHP inhibited hepatic p38 MAPK phosphorylation in animals with postburn sepsis.Conclusion Biopterin might play a role in p38 MAPK activation induced by postburn sepsis.
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