CAJ | 학술논문

目的探讨乌司他丁(UTI)对脂多糖(LPS)诱导小鼠的急性肺损伤(ALT)保护作用的可能机制.方法于小鼠腹腔注射LPS(10mg/kg)复制ALI动物模型.将小鼠随机分为对照组(A组,n=10)、LPS组(B组,n=10)、乌司他丁(Ulinastatin)+LPS组(C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核转录因子-kB(NF-kB)的表达,ELISA法检测肺匀浆中肿瘤坏死因子-α(TNF-α),白细胞介素-6(IL-6).结果病理学改变B组与A、C组比较,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,IL-6含量与A、C组比较明显增加,B组肺组织NF-kB的表达组与A、C组比较明显增加.结论 UTI通过抑制NF-kB、TNF-α、IL-6的表达减轻LPs所致急性肺组织损伤.
목적 탐토오사타정(UTI)대지다당(LPS)유도소서적급성폐손상(ALT)보호작용적가능궤제.방법 우소서복강주사LPS(10mg/kg)복제ALI동물모형.장소서수궤분위대조조(A조,n=10)、LPS조(B조,n=10)、오사타정(Ulinastatin)+LPS조(C조,n=10).관찰각조폐조직병이학개변,측량폐간/습(D/W)중비,용면역조직화학기술검측폐조직핵전록인자-kB(NF-kB)적표체,ELISA법검측폐균장중종류배사인자-α(TNF-α),백세포개소-6(IL-6).결과 병이학개변B조여A、C조비교,폐조직유경다백세포침윤화폐포벽결구적파배.B조폐조직중TNF-α,IL-6함량여A、C조비교명현증가,B조폐조직NF-kB적표체조여A、C조비교명현증가.결론 UTI통과억제NF-kB、TNF-α、IL-6적표체감경LPs소치급성폐조직손상.
Objective To investigate the protective effect of Ulinastatin (UTI) on acute lung injury induced by lipopolysaccharide (LPS) and its protective mechanism in mice.Methods The Kunming mice were randomly divided into sham group (group A,n =10),LPS group (group B,n =10),UTI +LPS group (group C,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 biopsy was used for examination of dry/wet (D/W) ratio to compare the levels of lung edema.The pathological changes in lung tissues were examined by light microscope.The NF-kB expression in pulmonary endothelium was assessed by immunohistochemical staining.The levels of tumor necrosis factor alpha ( TNF-α),interleukin-6 (IL-6) were detected by ELISA.Results Lung biopsy of rats in group B displayed more leukocytic infiltrate,pulmonary capillary congestion,interstital edema and intraalveolar hemorrhage than any other groups,The expressions of the NF-kB,IL-6 and TNF-α of group B were significantly higher than those of any other groups.Conclusions Ulinastatin can play a protective role against LPS-induced acute lung injury,through inhibiting the activation of NF-kB,and releasing of TNF-α,IL-6.