Liu Chang, Zhang Hong, Cheng Peng-yan, Zhou Fa-chun
Department of Critical Care Medicine, the First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Zhonghua Wei Zhong Bing Ji Jiu Yi Xue. 2013 Mar;25(3):159-63. doi: 10.3760/cma.j.issn.2095-4352.2013.03.010.
To observe the influence of pre-B-cell colony enhancing factor (PBEF) on intercellular cell adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) in lung tissue of rats with acute lung injury/acute respiratory distress syndrome (ALI/ARDS) induced by oleic acid.
A total of 40 male adult Sprague-Dawley (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 by injection 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 group received the same volume of the vehicle only. Six hours after ALI/ARDS was successfully reproduced, bronchoalveolar alveolar lavage fluid (BALF) was obtained for the measurement of the contents of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) by enzyme linked immunosorbent assay (ELISA). Lung tissue was obtained for pathological examination, and also for the measurement of the expression of PBEF, ICAM-1 and VCAM-1 mRNA by reverse transcription-polymerase chain reaction (RT-PCR), and also the protein levels of PBEF, ICAM-1 and VCAM-1 by immunohistochemistry.
Compared with rats in control group, the lung tissue of rats in model group showed distinctive pathological changes, the contents of TNF-α and IL-1β in BALF were increased (TNF-α: 656.51±47.13 ng/L vs. 84.82±7.84 ng/L, IL-1β: 379.60±31.55 ng/L vs. 74.56±8.51 ng/L, both P<0.01), the mRNA and protein expression of PBEF, ICAM-1 and VCAM-1 were significantly increased (PBEF mRNA: 0.581±0.079 vs. 0.186±0.051, ICAM-1 mRNA: 0.558±0.060 vs. 0.176±0.070, VCAM-1 mRNA: 0.646±0.059 vs. 0.226±0.047; PBEF protein: 0.089±0.024 vs. 0.037±0.011, ICAM-1 protein: 0.061±0.012 vs. 0.025±0.008, VCAM-1 protein: 0.072±0.013 vs. 0.033±0.010, all P<0.01). Compared with model group, amelioration of pathological change was found in lung tissue of rats in drug intervention group, the contents of TNF-α and IL-1β in BALF were reduced (TNF-α: 478.80±72.93 ng/L vs. 656.51±47.13 ng/L, IL-1β: 244.62±52.17 ng/L vs. 379.60±31.55 ng/L, both P<0.05), and the mRNA and protein expression of PBEF, ICAM-1 and VCAM-1 were lowered (PBEF mRNA: 0.456±0.110 vs. 0.581±0.079, ICAM-1 mRNA: 0.413±0.073 vs. 0.558±0.060, VCAM-1 mRNA: 0.483±0.062 vs. 0.646±0.059; PBEF protein: 0.059±0.010 vs. 0.089±0.024, ICAM-1 protein: 0.043±0.007 vs. 0.061±0.012, VCAM-1 protein: 0.050±0.009 vs. 0.072±0.013, all P<0.05).
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.
观察前B细胞集落增强因子（PBEF）对油酸诱导的急性肺损伤/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）和血管细胞黏附分子-1（VCAM-1）的影响。
将40只成年雄性Sprague-Dawley（SD）大鼠按随机数字表法分为对照组、模型组、药物干预组和溶剂对照组，每组10只。模型组、药物干预组和溶剂对照组大鼠经尾静脉注射油酸（0.15 ml/kg）复制ALI/ARDS模型。药物干预组和溶剂对照组大鼠给予特异性PBEF抑制剂FK866（10 mg/kg），溶剂对照组大鼠仅给予等量溶剂。成功复制ALI/ARDS 6小时后，采集支气管肺泡灌洗液（BALF），采用酶联免疫吸附测定（ELISA）法检测肿瘤坏死因子-α（TNF-α）和白细胞介素-1β（IL-1β）含量。取肺组织进行病理检查，采用逆转录-聚合酶链反应（RT-PCR）检测PBEF、ICAM-1和VCAM-1 mRNA表达，采用免疫组织化学法检测PBEF、ICAM-1和VCAM-1蛋白水平。
与对照组大鼠相比，模型组大鼠肺组织出现明显病理改变，BALF中TNF-α和IL-1β含量升高（TNF-α：656.51±47.13 ng/L比84.82±7.84 ng/L，IL-1β：379.60±31.55 ng/L比74.56±8.51 ng/L，均P<0.01），PBEF、ICAM-1和VCAM-1的mRNA和蛋白表达显著增加（PBEF mRNA：0.581±0.079比0.186±0.051，ICAM-1 mRNA：0.558±0.060比0.176±0.070，VCAM-1 mRNA：0.646±0.059比0.226±0.047；PBEF蛋白：0.
