中文摘要：

目的探讨地寒米松对氧化应激时H441细胞肺表面活性蛋白（surfactant protein．SP）A、B、C和D表达的影响。方法采用H2O2制作H441细胞氧化晦激模型。实验分为对照组、不同浓度地塞米松（1、10和100μmol／L）组、H2O2（100μmol／L）损伤组、H2O2（100μmol／L）±地塞米松（100μmol／L）组。共培养24h后采用实时荧光定量聚合酶链反应技术检测各组培养细胞中SP-A、B、C和DmRNA的表达水平，采用Western印迹技术榆测SPA、B、C和D蛋白的表达。多组间比较采用单因素方差分忻，并采用Dunnett’s T3检验进行两两比较。结果（1）H2O2损伤组SP-A mRNA表达水平明娃高丁对照组（4．0016±0．3618与0．9914±0．4170），向SP-C与SPD表达明显低于对照组（SP-C：0．2840±0．0586与0．9719±0．1022；SP—D：0．6199±0．0074与0．9518±0．0614），差异均有统计学意义（P均〈0．05）；与H2O2损伤组相比，H2O2±地寒米松组SPAmRNA的表达水平下降（2．5191±0．3463），而SP-D mRNA的表达水平升高（0．9076±0．0167）。差异均有统计学意义（P均〈0．05）。（2）H2O2损伤组SP-A蛋白表达水平明显高于对照组（2．1795±0．0645与0．9728±0．0090），SP-B、SP—C与SPD蛋白表达水平明显低于对照组（SP-B：0．2593±0．0086与0．7253±0．0134；SP-C：0．5592±0．0111与0．9472±0．0052；SP-D：1．1550±0．0237与1．2991±0．0298）；与H2O2损伤组相比，H2O2±地塞米松组SPA蛋白表达降低（1．4974±0．0185），而SP-B、SP-C与SP-D蛋白表达水平升高（0．7389±0．0182、0．9244±0．0282和1．3339±0．0136），筹砰均有统计学意义（P均〈0．05）。结论地塞米松可能通过调节SP的表达，对H441细胞氧化心激损伤发挥保护作用。

英文摘要：

Objective To explore the effects of dexamethasone on the expressions of surfactant protcin（SP） A, B, C and D in H441 cells injured the oxidative stress. Methods H441 cells were challenged with hydrogen peroxide as oxidative stress damage cell model. Then the cells were divided into control group, groups on differew, dexamethasone levels （1, 10 and 100 l, mol/L）, H2O2 （100 μmol/L） injury group and dexamethasone （100μmol/L）＋H2O2（100 μmol/L） group. All cells were cuhured for 24 hours, then the expressions of SP mRNA were analyzed by quantitative real time polymcrase chain reaction, and proteins were delected hyWestern blot. One way variant analysis and Dunnctt＇s T3 test were applied as statistical methods. Results （1） The mRNA level of SPA in H2O2 injury group was higher than thai in the control group （4. 0016±0. 3618 vs 0. ,9914±0. 4170） , while mRNA of SP-C and SP-D were lower than those in the control group （SP -C：0. 2840±0.0/586 vs 0.9719±0. 1022;SP-D：0.6199±0.0074 vs 0.9518±0.0614） （all P〈0.05）. Comtpared with H2O2 injury group, the mRNA level of SPA in dexamethasone ＋ H2O2 group was down regulated （2. 5191±0. 3463）, but SP-D mRNA was up-regulated （0. 9076±0. 0167） （all P〈0.05）. （2） The SPA protein level in H2O2 injury group was higher than that in the control group （2. 1795±0. 0645 vs 0. 9728±0. 009）,while SP B,SP C and SP D protein levels were lower than those in the control group （SP-B：0. 2593±0. 0086 vs 0. 7253±0. 0134;SP-C：0. 5592±0.0111 vs 0. 9472±0. 0052;SP-D： 1. 1550±0.0237 vs 1.2991±0.0298）. Compared with H2O2 injury group, the protein level of SPA in dexamethasone＋H2O2, group was down-regulated（1.4974±0.0185）,while SP-B, SP-C and SP D levels were up regulated （0. 7389±0. 0182, 0. 9244±0. 0282 and 1. 3339±0. 0136）. The differences were statistically significant respectively （all P〈0.05）. Conclusions Dexamethasone may protect H441 cells from being damaged by H2O2 through regulating SP m