摘要
目的 观察急性肺损伤 (ALI)肺组织核因子 (NF) -κB、肿瘤坏死因子 (TNF) -α的活性变化及地塞米松 (Dex)的干预作用。方法 采用ALI大鼠模型 ,实验动物随机分为ALI模型组 (8只 )、Dex治疗组 (8只 )、正常对照组 (8只 ) ,用免疫组织化学法结合原位定量分析检测肺组织NF -κB、IκB -a、TNF -α蛋白表达及相对含量 ,并进行肺组织的病理学光镜检查。结果 ALI大鼠肺组织NF -κB、TNF -α的蛋白表达明显升高 ,I-κB表达显著降低。Dex能明显下调NF -κB、TNF -α的蛋白表达 ,上调I-κB表达 ,并能减轻肺组织的损伤程度。结论 NF -κB活化在ALI的发生、发展过程中起着重要作用。Dex发挥抗炎作用 ,减少肺组织损害 ,与其对NF -κB的活性和细胞因子的调节作用密切相关。
Objective To investigate the activation changes of nuclear factor-κB (NF-κB) and the tumor necrosis factor-α(TNF-α) in the lung tissue on acute lung injury (ALI) with the effect of dexamethasone(Dex). Methods ALI rats model was made by injection of lipopolysaccharide (LPS) intravenously. Rat models of ALI were used in this study. Rats were randomly divided into the normal control group (n=8),ALI model group (n=8) and Dex treatment group (n=8). By using immunohistochemistry combined with in situ quantitative analysis, the distribution and relative contents of NF-κB, IκB-a and TNF-α in lung were determined. The pathological changes were examined with light microscope in the lung tissues. Results In ALI model group, the expressions of NF-κB and TNF-α increased,whereas the expression of IκB-a decreased. In the dexamethasone treatment group, the expression of NF-κB and TNF-α were down-regulated and IκB-a was up-regulated and relieve the lung injury observed by histological examination. Conclusions NF-κB activation may play an improtant roles in development and progression of ALI. Dex could show antiinflammatory effect and relieve the lung injury in ALI, which was contributed to the regulatory roles of Dex on the NF-κB activation and cytokine cecretion.
出处
《中国急救医学》
CAS
CSCD
北大核心
2002年第9期497-498,共2页
Chinese Journal of Critical Care Medicine
基金
国家自然科学基金资助项目 (3 0 0 0 0 165 )
