脂多糖致大鼠急性肺损伤早期Ⅰ型前胶原羧基端肽的表达

目的：观察脂多糖（LPS）致大鼠急性肺损伤（ALI）早期是否存在肺纤维增生,探讨其在ALI发病机制中的作用。方法：将27只SD大鼠随机分成3组,其中对照组为气管内滴注NS（生理盐水）12h后取材,LPS1组、LPS2组为气管内滴注LPS 1.0ml/kg（浓度为100μg/ml）后分别于12h、24h取材。用酶联免疫吸附试验（ELISA）方法测定血清及肺泡灌洗液（BALF）中Ⅰ型前胶原羧基端肽（PⅠCP）的浓度。结果：LPS2组大鼠血清PⅠCP浓度为（64.75±11.97）μg/L显著高于对照组（12.38±3.59）μg/L和LPS1组（13.96±4.30）μg/L（P〈0.05）,而LPS1组和对照组间差异无显著性（P〉0.05）;LPS2组大鼠BALF中PⅠCP浓度为（35.26±3.32）μg/L显著高于对照组（6.90±1.99）μg/L和LPS1组（6.92±2.50）μg/L（P〈0.05）,而对照组和LPS1组间差异无显著性（P〉0.05）。结论：LPS致大鼠ALI后24h血清及BALF中PⅠCP浓度显著增高提示ALI早期肺纤维增生存在。

Expression of Type Ⅰ Procollagen Peptide in Rat with Early Acute Lung Injury Caused by Lipopolysacharide

Objective：To observe the fibroproliferation occurs early in the acute lung injury （ALl）caused by lipopolysacharide （LPS）. Methods： Twenty-seven SD rats were divided into 3 groups randomly, the control group was instilled saline into trachea for 12h; and the lung samples were made. The LPSI group and LPS2 group were instilled LPS 1.0 ml/kg（100μg/ml） for 12h and 24h respectively, and the lung samples were made. Type Ⅰ procollagen peptide（ P Ⅰ CP） was detected by ELISA in serum and bronchoalveolar lavage fluid（BALF）. Results：The serum P I CP concentration in LPS2 group （64. 75 ± 11.97） μg/L,was significantly higher than that in control group（ 12.38 ± 3.59 ） μg/L and LPSI group（ 13.96 ± 4. 30） μg/L （P 〈 0. 05 ）. Control group and LPS, group had no significant difference（P 〉0. 05）. The BALF P Ⅰ CP concentration in LPS2 group（35.26±3.32） μg/L,was significantly higher than that in control group（6.90 ±1.99） μg/L and LPSt group（6. 92 ±2. 50） μg/L （P 〈0. 05）. Control group and LPStgroup had no significant difference（P 〉0. 05）. Conclusions： The significant increase of P Ⅰ CP in serum and BALF after 24h in ALl caused by LPS indicate the existence of lung fibroproliferation.