幼鼠肠缺血再灌注损伤时TNF-α的产生及作用

Source and Effects of Tumor Necrosis Factor-α in Model of Imma ture Rats With Ischemia /Reperfusion Injury of Gut

目的 :探讨肠缺血 /再灌注时肿瘤坏死因子 α(tumornecrosisfactor α ,TNF α)的来源及作用。方法 :建立幼鼠肠缺血 /再灌注动物模型 ,利用放射免疫法检测门静脉和外周血血清中TNF α表达及对肠组织进行形态学观察。结果 :缺血 30min组肠粘膜轻度受损 ,缺血 30min /再灌注 30min组、缺血 30min/再灌注 6 0min组、缺血 30min/再灌注 90min组肠粘膜中度受损 ,缺血 12 0min组肠粘膜重度受损。肠缺血 30min组门静脉血清TNF α开始升高为 (2 .0 6± 0 .5 2 )ng/ml,缺血 30min/再灌注 30min组达峰值为 (2 .96± 0 .4 5 )ng/ml,二者皆明显高于对照组 (P <0 .0 5 ) ;缺血 30min/再灌注 6 0min组、缺血 30min/再灌注 90min组时下降 ;肠缺血 30min/再灌注 30min组外周血清TNF α也升高为 (2 .11± 0 .2 9)ng/ml(P <0 .0 5 )。且缺血 30min组、缺血 30min/再灌注 30min组、缺血 12 0min组门静脉TNF α水平显著高于外周血 (P <0 .0 5 )。结论 :幼鼠肠缺血 /再灌注后TNF α在肠、肝内均有产生 ,但门静脉血清TNF α较外周血血清升高明显 ,因此推论幼鼠肠缺血 /再灌注损伤TNF α可能主要来源于肠组织 ,并且介导幼鼠肠缺血

﨩bjective: [WT5'BZ] Our aim was to investigate the sour ce and effects of tumor necrosis factor α (TNF α) in the model of immature rat after ischemia / reperfusion (I/R) injury of gut. [WT5'HZ]Methods: [WT5 'BZ] We stained the gut with hematoxylin and eosin and observed the pathologic changes. The serum concentrations of TNF α were determined by using radioimmun oassay(RIA) with a TNF α RIA kit of rats. [WT5'HZ]Results: [WT5'BZ] The m ucosal villi of gut were weakly damaged with edema in ischemia 30 minute group; and more seriously damaged with necrosis or hemorrhage in ischemia 30 minute /r eperfution 30 minute group and ischemia 120 minute group. The TNF α in the p ortal increased in ischemia 30 minute group (2.06±0.52)ng/ml. The levels of T NF α reached peak in ischemia 30 minute /reperfution 30 minute group (2.96 ±0.45)ng/ml, decreased in ischemia 30 minute /reperfution 60 minute group,and reached the basal line in ischemia 30 minute /reperfution 90 minute group. Mo reover, the levels of TNF α of portal serum were significantly higher than tho se of systemic serum in ischemia 30 minute group, ischemia 30 minute /reperfut ion 30 minute group, ischemia 120 minute group(P<0.05). [WT5'HZ]Conclusio n: [WT5'BZ]The gut might be the major source of TNF α, which mediates the ischemia/reperfution injury of gut [WT5'HZ]