前B细胞克隆增强因子对急性肺损伤/急性呼吸窘迫综合征大鼠肺组织细胞豁附分子的影响

刘畅，张虹程，鹏雁，周发春.前B细胞克隆增强因子对急性肺损伤/急性呼吸窘迫综合征大鼠肺组织细胞豁附分子的影响[J].中华危重病急救医学.2013,25(3),1

前B细胞克隆增强因子，细胞阳j载附分子一I，皿管细胞薪附分子一1，急性肺损伤

刘畅，张虹程，鹏雁，周发春

重庆医科大学附属第一医院重症医学科

2013

159-163

知网

观察前B细胞克隆增强因子(PBEF)对急性肺损伤/急性呼吸窘迫综合征(ALI/ARDS)大鼠肺组织细胞间黏附分子-1(ICAM-1)、血管细胞黏 附分子-1(VCAM-1)的影响.方法 将40只SD大鼠按随机数字表法分为对照组、模型组、药物干预组、溶媒对照组,每组10只.采用油酸尾静脉注射复制ALI/ARDS模型.药物干预组制模 前腹腔内注射PBEF抑制剂FK866,溶媒对照组制模前注射等体积FK866溶媒二甲亚砜.制模成功6h后取材,采用酶联免疫吸附试验(ELISA)测 定支气管肺泡灌洗液(BALF)中肿瘤坏死因子-α(TNF-α)、白细胞介素-1β(IL-1β)含量；观察肺组织病理学变化；用逆转录-聚合酶链反应 和免疫组化染色测定肺组织中PBEF、ICAM-1、VCAM-1的mRNA及蛋白表达.结果 与对照组比较,模型组大鼠肺组织出现明显的ALI/ARDS病理学改变,BALF中TNF-α (ng/L)、IL-1β (ng/L)含量增多(TNF-α:656.51±47.13比84.82±7.84,IL-1β:379.60±31.55比74.56±8.51,均 P＜0.01),PBEF、ICAM-1、VCAM-1的mRNA和蛋白表达增加(PBEF mRNA:0.581±0.079比0.186±0.051,ICAM-1 mRNA:0.558±0.060比0.176±0.070,VCAM-1mRNA:0.646±0.059比0.226±0.047；PBEF蛋 白:0.089±0.024比0.037±0.011,ICAM-1蛋白:0.061 ±0.012比0.025±0.008,VCAM-1蛋白:0.072±0.013比0.033±0.010,均P＜0.01).与模型组比较,药物干预 组大鼠肺组织病理改变有所减轻,BALF中TNF-α、IL-1β含量显著降低(TNF-α:478.80±72.93比656.51 ±47.13,IL-1β:244.62±52.17比379.60±31.55,均P＜0.05),PBEF、ICAM-1、VCAM-1的mRNA和 蛋白表达明显减少(PBEF mRNA:0.456±0.110比0.581±0.079,ICAM-1 mRNA:0.413±0.073比0.558±0.060,VCAM-1 mRNA:0.483±0.062比0.646±0.059；PBEF蛋白:0.059±0.010比0.089±0.024,ICAM-1蛋 白:0.043±0.007比0.061±0.012,VCAM-1蛋白:0.050±0.009比0.072±0.013,均P＜0.05).结论 在ALI/ARDS发生时PBEF能通过增加黏附分子ICAM-1、VCAM-1表达促使炎性细胞向肺内迁移和浸润,从而在其发生发展中起重要作用。 To observe the influence of pre-B-cell colons enhancing factor PBEF on intercellular cell adhesion molecule-1(IC A\1-1)and rascular cell adhesion molecule-1(一 C AEI-1)in lung tissue of rats with acute lung injury/acute respiratory distress syndrome(I,IL9RDS) induced by oleic acid. Methods A total of 40 male adult Sprague-Dawlev(sD)rats were divided into control, model, drug intervention and vehicle control groups according to the random digits table with 10 rats in each group. ALI/ARDS was reproduced in the rats of model, drug intervention and vehicle control groups 1injection of oleic acid (0.15 ml/kg)through the tail vein. The rats in drug intervention and vehicle control groups received the specific PBEF inhibitor FK866(10 mg/kg)，while vehicle control a-oup received the same volume of the vehicle only=. 5is hours after- ALl/ARDS was successfully reproduced, bronchoalveolar alveolar lavage fluid(BALF ) was obtained for the measurement of the contents of tumor necrosi, factor-a l TNF-a ) and interleuki，卜1日(IL-1日)by enzyme linked immunosorbent assay(ELIS A).Lung tissue was obtained for pathological examination, and also for the measurement of the expression of PBEF, ICAM-1 and VCAM一I rnRNA by reverse transcription-polvmerase chain reaction(R'f-PCR)，and also the protein levels of PBEF, ICAM-1pathological change was found in lung tissue of rats in drug intervention group, the contents of TNF-a and IL-1(3 inBALF were reduced ( TNF-a:478.80士72.93 vs. 656.51士47.13，IL-1日:244.62士52.17 vs. 379.60士31.55，bothP < 0.05)，and the mRNA and protein expression of PBEF, ICAM-1 and VCAM-1 were lowered (PBEF mRNA;0.456士0.110 vs. 0.581士0.079，ICAM-1 mRNA: 0.413士0.073 vs. 0.558士0.060, VCAM-1 mRNA: 0.483士0.062vs. 0.646士0.059; PBEF protein: 0.059士0.010 vs. 0.089士0.024, ICAM-1 protein: 0.043士0.007 vs. 0.061士0.012,VCAM-1 protein: 0.050士0.009 vs. 0.072士0.013，all P < 0.05).Conclusion PBEF could aggravate migration of pro-inflammatory cells to infiltrate the lung tissue by increasing the expression of ICAM-1 and VCAM-1, thus it plays an important role in the development of ALI/ARDS.and VCAM-1 by immunohistochemistry. Results Compared So0ith rats in control group, the lung tissue of rats in model group showed distinctive pathological changes, the contents of TNF-a(ng/L ) and 11一1(3 (ng/L) in BALE were increased ('fNF-x:656.51士47.13、、.84.82士7.84. IL-1p:379.60士31.55、*.74.56士8._51，both P