p38丝裂原活化蛋白激酶抑制剂对大鼠急性肺损伤血清及支气管肺泡灌洗液中细胞因子的影响

Effect of p38MAPK inhibitor pretreatment on cytokins in serum and bronchoalveolar larage fluid in rats with acute lung injury

目的探讨p38丝裂原活化蛋白激酶(MAPK)抑制剂治疗内毒素型急性肺损伤(ALI)的机制。方法腹腔内注射+气管内给内毒素复制大鼠ALI模型。用酶联免疫吸附试验测定血清及肺泡灌洗液中肿瘤坏死因子α(TNF-α)、白细胞介素6(IL-6)及IL-10水平。结果大鼠血清和支气管肺泡灌洗液中TNF-α、IL-6含量,实验组和预处理组显著高于对照组(P<0.01),实验组高于预处理组(P<0.05);血清和支气管肺泡灌洗液中IL-10含量,实验组和预处理组高于对照组(P<0.01),而实验组和预处理组之间无显著性差异。结论TNF-α、IL-6和IL-10在大鼠内毒素ALI过程中可能起重要作用。p38MAPK抑制剂可能通过抑制TNF-α、IL-6过度分泌而减轻肺损伤。

Objective To investigate the mechanism of therapeutic effect of p38MAPK inhibitor on acute lung injury （ALI）. Methods ALI model of rats was established by injecting lipopolysaccharide（LPS） to the abdominal cavity and trachea and BLISA assay was used for detecting the levels of TNF-α,IL-6 and IL-10 in serum and bronchoalveolar larage fluid （BALF）. Results The levels of TNF-α, IL-6 in serum and BALF in experiment and pretreatment groups were significantly higher than those in control group（P〈0. 01）, which in the expriment group were significantly higher than those in the pretreatment group（P〈0. 05）. The level of IL-10 in serum and BALF in the experiment and pretreatment groups were significantly higher than those in the control group（P〈 0. 01）,which were not remarkably different between the experiment group and pretreatment group. Conclusions TNF-α,IL-6 and IL-10 may play important roles in the process of LPS-induced ALl in rats. p38MAPK inhibitor may relieve lung injuries by inhibiting excessive discharging of TNF-α and IL-6.