论文部分内容阅读
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 observe the changes of nuclear factor (NF) -κB activity in lungs of acute lung injury (ALI) and the effect of Dex. Methods Thirty SD rats were randomly divided into experimental group (ALI + Dex, 10 rats), model group (ALI + NS, 10 rats) and control group (NS rats) with LPS-induced acute lung injury Three groups were given intraperitoneal injection of dexamethasone after successful modeling. The model group was injected intraperitoneally with the same dose of normal saline after successful modeling, while the control group was injected intraperitoneally with the same dose of normal saline. Six hours after injection, lung tissues were collected, and the relative contents of NF-κB P65 and IκB-α protein were detected by immunohistochemical method and image analyzer. Pathological light microscopy was performed. Results A large number of hemorrhage and inflammatory cell infiltration were found in the lung tissue of ALI rats. The protein expression of NF-κBp65 was significantly increased and the expression of IκB-α was significantly decreased. Dex can significantly down-regulate the protein expression of NF-κBp65, up-regulate the expression of IκB-α, and reduce the degree of lung injury. Conclusion The activation of NF-κB P65 plays an important role in the development of ALI. Dex has a significant anti-inflammatory effect, reducing lung tissue damage.