抗肿瘤坏死因子抗体减轻体外循环的肺损伤  被引量:3

The experimental study of intratracheal administration of anti-tumor necrosis factor-α antibody attenuating lung injury after cardiopulmonary bypass

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作  者:于洋[1] 祁丹妮[2] 韦华[1] 胡晖[1] 刘晓[1] 顾承雄[1] 

机构地区:[1]首都医科大学附属北京安贞医院心脏外科,100029 [2]哈尔滨医科大学微生物教研室

出  处:《中华胸心血管外科杂志》2007年第5期338-341,共4页Chinese Journal of Thoracic and Cardiovascular Surgery

基  金:北京市优秀人才培养基金资助(20061D0300600084)

摘  要:目的探讨气管内给予抗肿瘤坏死因子抗体(TNF-α Ab)对体外循环(CPB)肺损伤的保护作用及机制。方法选取健康家兔28只,随机分为单纯开胸组、单纯 CPB 组、CPB+经气管插管注入生理盐水组和 CPB+TNF-α Ab 组(术前和主动脉开放后经气管插管注入抗兔 TNF-α Ab,总量2400 pg/kg)。测定各组围 EPB 期左、右心房血液中中性粒细胞计数、肿瘤坏死因子(TNF-α)和丙二醛(MDA)的含量;取肺组织样本,电镜观察其超微结构,并观察肺组织含水量、TNF-α mRNA 和 TNF-α蛋白的表达及细胞凋亡情况。结果 TNF-α Ab 明显抑制 CPB 期间中性粒细胞在肺内的聚集,抑制肺源性 TNF-α的释放,减少脂质过氧化物的终产物 MDA 的产生。同时,TNF-α Ab 还可降低肺含水量,减少肺组织细胞凋亡的发生,且肺组织病理形态学改变较轻,但并未从转录水平及蛋白水平上减少 TNF-α的分泌。结论气管内应用TNF-α Ab 能明显减轻体外循环肺损伤。Objective To study the protective effect and its mechanism of anti-tumor necrosis factor-α antibody (TNF-α Ab) on lung injury after cardiopulmonary bypass(CPB). Methods Twenty-eight healthy rabbits were selected and randomly divided into four groups: group Ⅰ only received open chest operation; groups Ⅱ -Ⅳ underwent CPB. In the group Ⅳ, rabbit TNF-α Ab (2 400 pg/kg) was dropped into the intracheal tube before operation and just after releasing the aortic clamp. Saline was given to the group Ⅲ instead. Blood neutrophils count, TNF-α, MDA from the right and left atrium in the four groups were determined perioperatively. Water volume, TNF-α mRNA, TNF-α protein, apoptosis and pathomorphological changes were measured in the lung tissues. Results TNF-α Ab can restrain leukocyte accumulation, reduce releasing of TNF-α and MDA in the lung. It can also reduce the occurrence of apoptosis and attenuate pathomorphological changes in the lung tissue. However, it cannot reduce the secretion of TNF-α at the transcription level and protein level. Conclusion Intratracheal TNF-α Ab administration has markedly protective effect on lung injury after CPB.

关 键 词:体外循环 细胞凋亡 肺/损伤 抗肿瘤坏死因子抗体 肺保护 

分 类 号:R654.1[医药卫生—外科学]

 

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