地塞米松对脓毒症大鼠急性肺损伤影响的实验研究

Effects of dexamethasone on acute lung injury in sepsis rats

目的 观察急性肺损伤(ALI)肺组织核因子(NF)-κB的活性变化及地塞米松(Dex)的干预作用。方法 采用LPS诱导的急性肺损伤动物模型,将30只SD大鼠随机分为实验组(ALI+Dex,10只)、模型组(ALI+NS,10只)和对照组(NS,10只)三组,实验组在建模成功后腹腔注射地塞米松,模型组在建模成功后腹腔注射相同剂量的生理盐水,对照组仅腹腔注射相同剂量的生理盐水。注药6小时后留取肺组织,用免疫组织化学法结合图像分析仪检测其NF-κBP65、IκB-α蛋白的相对含量,并进行病理学光镜检查。结果 ALI大鼠肺组织可见大量出血和炎性细胞浸润,NF-κBP65的蛋白表达明显升高,IκB-α表达显著降低。Dex能明显下调NF-κBP65的蛋白表达,上调IκB-α表达,并能减轻肺组织的损伤程度。结论 NF-κBP65活化在ALI的发生、发展过程中起着重要作用。Dex具有明显的抗炎作用,减少了肺组织损害。

Objective To investigative the activation changes of nuclear factor-κB(NF-κB) in the lung tissue on acute lung injury(ALI) and the effect of dexamethasone(Dex). Methods ALI rat models were given the intraperitoneal injection of lipopolysaccharide(LPS). 30 SD rats were randomly average divided into three groups: experimental group(ALI+Dex)、model group (ALI+NS,n=10) and control group(NS, n= 10). Dex and saline were immediately injected intraperitoneally in experimental group and model group respectively. Control group were injected with only same dose of saline. All rats were killed and the specimens of lung tissues were reserved 6 hours after injected. The content of NF-κ BP65,IκB-α were detected by image analyse system and immunohistochemistry. The pathological changes of the lung tissues were examined with light microscope. Results In ALI model group, neutro-phil infiltration and hemorrhage in the cavity of alveolus were found; the expression of NF-κBP65 increased, IκB-α decreased. In the Dex treatment groups that the expression of NF-κBP65 was down-regulated and IκB-α was up-regulated and relieve the lung injury observed by histological examination. Conclusion Dex have prominently anti-inflammatory effect and can relieve the lung injury in ALI rats indued by LPS.