地塞米松对急性肺损伤大鼠肺组织iNOS mRNA表达的影响

The Influence of Dexamethasone on the Acutely Injured Lung and the Potential Mechanisms

目的 观察地塞米松对内毒素性急性肺损伤肺组织的影响 ,并探讨其机制。方法 30只SD大鼠随机分为 3组 ,即正常对照组、损伤组和地塞米松组。用内毒素复制急性肺损伤模型 ,地塞米松组同时注射内毒素和地塞米松 ,注射后 2h处死动物。观察形态学变化并分别测定一氧化氮 (NO)和丙二醛 (MDA)的含量 ;用原位杂交方法检测各组大鼠肺组织中诱导型一氧化氮合酶mRNA(iNOSmRNA)的表达水平。结果 损伤组肺组织MDA、NO含量和iNOSmRNA表达量较正常对照组显著增加 (P <0 .0 5 ) ;地塞米松组肺组织MDA、NO含量和iNOSmRNA表达量明显低于损伤组 (P <0 .0 5 )。结论 内毒素性急性肺损伤时 ,肺组织iNOSmRNA大量表达 ,导致内源性NO爆发式产生 ,从而介导肺损伤。

Objective To investigate the influence of dexamethasone on acute endotoxic lung injury and the potential mechanisms.Methods Duplicate the acute lung injury model with 5mg/kg endotoxin, 10mg/kg dexamethasone and 5mg/kg endotoxin were injected at the same time for the dexamethasone treatment group. All the animals were killed at the timepoint of 2h. Detect the content of NO, MDA and the expression level of iNOS mRNA in the lung tissue accordingly.Results After 2h's treatment with lipopolysaccharide (LPS), (1) the content of MDA, NO and iNOS mRNA level increased remarkably(P<0.05). (2) after treatment with dexamethasone, the content of NO, MDA and the level of iNOS mRNA decreased significantly compared with the injured groups.Conclusions In the endotoxic acute lung injury, large amounts of iNOS mRNA expressed in the lung, which caused the outbreak of endogenic NO and subsequently mediated lung injury, while dexamethasone could inhibit the injury.