地塞米松对急性肺损伤肺组织中foxml基因的作用

Influence of dexamethasone on foxml gene expression in pulmonary tissue following acute lung injury

目的 探讨脂多糖（lipopolysaccharide,LPS）内毒素所致的小鼠急性肺损伤（acute lung in-jury,ALI）时肺组织foxml转录因子和foxml基因表达及其在ALI中的保护作用,并观察地塞米松（dex-amethasone,DEX）对foxml基因表达和病情转归的影响.方法 72只健康小鼠随机（随机数字法）分为3组：对照组（A组,n=24）,模型组（B组,n=24）,地塞米松治疗组（C组,n=24）.对照组小鼠腹腔注射0.9%生理盐水（0.3 mL）.模型组小鼠腹腔注射LPS（5 mg/kg）.地塞米松治疗组小鼠腹腔注射u）s（5 mg/kg）,6 h后腹腔注射地塞米松（5 mg/kg）,三组分别选取24 h,48 h,72 h三个观测点.免疫组织化学方法检测各组小鼠肺组织foxml蛋白的表达,应用逆转录聚合酶链式反应（RT-PCR）方法检测各组小鼠肺组织foxml基因的表达强度,并观察肺组织病理变化.结果 组间比较,在24 h,48 h,72 h时,模型组小鼠肺组织foxml mRNA与foxml蛋白均显著高于对照组（P〈0.05）,地塞米松治疗组小鼠肺组织foxml mRNA与foxml蛋白均显著高于模型组（P〈0.05）;组内比较,在48 h无论模型组和地塞米松治疗组小鼠肺组织foxml mRNA与foxml蛋白均达到高峰,48 h小鼠肺组织foxml mRNA与foxml蛋白显著高于72 h（P〈0.05）,72 h显著高于24 h（P〈0.05）.地塞米松治疗组和模型组比较,肺组织病理改变明显减轻.结论 在模型组和地塞米松治疗组,肺组织中foxml mRNA和foxml蛋白均明显增加.地塞米松通过促进肺组织中foxml mRNA和foxml蛋白表达,修复受损的内皮细胞和上皮细胞,减轻肺损伤的程度.

Objective To study the foxml gene and its protective effect on the lung tissue of rats with acute lung injury （ALI） induced by lipopolysaccharide （LPS）, and to observe the dexamethason＇ s （DEX） impacts on foxml gene and the prognosis of ALI. Method Seventy-two healthy mice were randomly（random number） divid-ed into three groups： control group （A group, n = 24）, model group （B group, n = 24） and DEX treatment group （C group, n = 24）. The observing intervals were respectively set in 24 h, 48 h and 72 hours. At each ob-serving interval, the foxml protein in lung tissue of mice was detected by using immunohistochemistry （IHC）, and the expression of foxml gene in lung tissue was detected by using RT-PCR, as well as to observe the pathological changes in lung tissue. Results Comparisons were made between paired groups at 24 h,48 h and 72 h intervals in which the expression of foxml mRNA and the level of foxml protein in lung tissue of mice in C group were signifi-cantly higher than those in B group （P 〈 0.05）, and those in B group were significantly higher than those in A group （P 〈 0.05）. The expression of foxml mRNA and the level of foxml protein in lung tissue of mice in B group at 48 h interval were significantly higher than those both at intervals of 72 h and 24 h （P 〈 0.05）, and the those at 72 interval were significantly higher than those at 24 h interval （P 〈 0.05）. Compared with B group, the pathologi-cal changes in lung tissue of mice in C group were lessened. Conclusions In both model group and dexamethasone treatment group, the expression of foxml mRNA and the level of foxml protein in lung tissue of mice are increased significantly. Dexamethasone lessens the injury of both vascular endothelial cells and alveolar epithelial ceils of lung tissue, and it also significantly increases the expression of foxml mRNA and the level of foxml protein.