模拟失重对肺组织iNOS表达的影响及地塞米松的防治作用

EFFECT OF SIMULATED WEIGHTLESSNESS ON iNOS IN PULMONARY TISSUES AND PROTECTIVE FUNCTION OF DEXAMETHASONE

目的研究尾悬吊模拟失重大鼠肺组织诱导型一氧化氮合酶(inducible nitric oxide synthase,iNOS)表达的变化及地塞米松对这一变化的影响。方法采用尾悬吊模拟失重,分为悬吊7、21 d及相应对照组和地塞米松干预组,每组10只,共50只大鼠。采用免疫组织化学技术检测肺组织iNOS的表达情况,采用原位杂交技术检测肺组织iNOSmRNA的表达情况,并观察应用地塞米松干预后肺组织iNOS的表达情况。结果同对照组相比,7 d尾悬吊模拟失重大鼠肺组织iNOS的表达水平明显增高(P<0.05),21 d尾悬吊模拟失重大鼠肺组织iNOS的表达水平亦显著增高(P<0.05),同时血管内皮阳性细胞数目显著增多(P<0.01)。7 d尾悬吊模拟失重大鼠肺组织iNOSmRNA的表达水平明显增高(P<0.01),21 d尾悬吊模拟失重大鼠肺组织iNOSmRNA的表达水平也显著增高(P<0.01)。地塞米松干预后大鼠肺组织iNOS的表达明显减低(P<0.05)。结论模拟失重可使肺组织iNOS活性增强,这可能是模拟失重造成肺损伤的重要机制之一,地塞米松可用于抑制模拟失重时肺组织一氧化氮的产生过程。

Objective To investigate the changes of inducible nitric oxide synthase（iNOS） in pulmonary tissues of tail-suspended rats during simulated weightlessness and the effect of dexamethasone. Methods Experiments were conducted on 50 Spragno-Dawley male rats, divided into 5 groups： suspended for 7 d, control of 7 d and suspended for 21 d, control of 21 d and dexamethasone treatment. Tail-suspension（-30^o） was used as weightlessness simulation, iNOS in pulmonary tissues was examined by immunohistochemistry and iNOSmRNA in pulmonary tissues was examined by hybridization in situ. Results The level of iNOS in pulmonary tissues of 7 d and 21 d tail-suspended rats was all increased significantly（ P〈0.05）. And the level of iNOSmRNA in pulmonary tissues of 7 d and 21 d tail-suspended rats increased significantly（ P〈0.01）. While the level of iNOS in the pulmonary tissues after dexamethasone treatment decreased significantly than that in tail-suspension group（ P〈0.05）. Conclusion Nitric oxide participated in the course of pulmonary tissue damage under simulated weightlessness condition. Simulated weightlessness can cause iNOS in pulmonary tissues increasing expression, which probably is an important mechanism of simulated weightlessness induced lung damage. Dexamethasone can be used as inhibiting nitric oxide expression in pulmonary tissues during simulated weightlessness.