摘要
目的:探讨褪黑素(MT)对大鼠急性肺损伤(ALI)时肺脏的保护作用及其可能机制。方法:将大鼠随机分为4组:对照组;脂多糖(LPS)组;地塞米松(DEX)和MT处理组。各组动物分别于气道内滴注后3、6和12h检测肺组织髓过氧化物酶(MPO)和超氧化物歧化酶(SOD)活性及丙二醛(MDA)含量;免疫组化检测细胞间黏附分子-1(ICAM-1)在肺组织的表达。结果:LPS组SOD活性较对照组明显降低(P<0.01),而MPO活性与MDA含量以及ICAM-1的表达则显著升高(P<0.01);应用MT及DEX均显著缓解上述变化(P<0.05或P<0.01)。结论:MT对ALI时的肺脏起明显的保护作用,其机制可能与MT清除自由基及抑制ICAM-1的表达有关。
Aim： To investigate the protective effect of melatonin（MT） on lung tissues during acute lung injury（ALI） in rats and its possible mechanism Methods： All rats were randomly divided into four groups： control group, lipopolysaccharide （LPS） group, dexamethasone（DEX） and MT treatment group. Myeloperoxidase （MPO） activity, superoxide dismutase （SOD） activity and malonaldehyde（MDA） content of lung tissues were detected at 3,6 and 12 h after intratracheal instillation in each group. In addition, the expression of intercellular adhesion molecule-1 （ ICAM-1 ） were observed through immunohistochemistry staining in lung tissues. Results： Compared with control group, SOD activity decreased significantly in LPS group（P〈 0.01）, but MPO activity, MDA content and the expression of ICAM-1 increased obviously（P 〈 0.01 ）. The administration of MT and DEX mitigated above changes significantly（P 〈 0.05 or P 〈 0.01）. Conclusion： MT possessed protective effect on lung tissues during ALI through scavenging free radicals and inhibiting the expression of ICAM-1 probably.
出处
《中国应用生理学杂志》
CAS
CSCD
北大核心
2008年第4期464-467,I0011,共5页
Chinese Journal of Applied Physiology
基金
河北省科技厅资助项目(04276101D-45)
