摘要
目的探讨还原型谷胱甘肽对内毒素诱导小鼠的急性肺损伤保护作用的可能机制。方法于小鼠腹腔注射LPS(10 mg/kg)复制ALI动物模型。将小鼠随机分为对照组(n=10)、LPS组(n=10)、还原型谷胱甘肽(GSH)+LPS组(n=10)。观察各组肺组织病理学改变,测量肺干/湿(D/W)重比,用免疫组织化学技术检测肺组织NF-κB的表达,ELISA法检测肺匀浆中TNF-α和IL-6。结果病理学改变B组与A,C组比较的肺组织有更多白细胞浸润和肺泡壁结构的破坏。B组肺组织中TNF-α和IL-6含量与A和C比较明显增加,B组肺组织NF-κB的表达组与A和C组比较明显增加。结论 GSH通过抑制NF-κB、TNF-α和IL-6的表达减轻LPS所致急性肺组织损伤。
【Objective】 To determine the protective effect of reduced glutathione(GSH) on acute lung injury induced by lipopolysaccharide(LPS) and its protective mechanism in mice.【Methods】 The Kunming mice were randomly allocated into sham(n =10),LPS groups(n =10),GSH+LPS groups(n =10).LPS was intraperitoneally injected at a dose of 10 mg/kg body weight in the LPS group,along with equal volumes of saline in the sham group.Lung biopsies were used for examination of dry/wet(D/W) ratio to compare the levels of lung edema.The pathological changes were examined with light microscope in lung tissues.The NF-κB expression in pulmonary endothelium was assessed by immunohistochemical staining.The level of tumor necrosis factor alpha(TNF-α),inter1eukin-6(IL-6) was detected by ELISA.【Results】 Lung biopsies of rats in group B displayed more leukocytic infiltrate,pulmonary capillary congestion,interstital edema and intraalveolar hemorrhage than those of any other groups,The expressions of the Nuclear factor-κΒ(NF-κB) and TNF-α of group B were significantly higher than those of any other groups.【Conclusions】 Reduced glutathione can play a protective role against LPS-induced acute lung injury,through inhibiting the activation of NF-κB,and release of TNF-α,IL-6.
出处
《中国现代医学杂志》
CAS
CSCD
北大核心
2011年第19期2247-2249,共3页
China Journal of Modern Medicine
关键词
还原型谷胱甘肽
内毒素
肺损伤
reduced glutathione
lipopolysaccharide
lung injury