中国急救医学
中國急救醫學
중국급구의학
CHINESE JOURNAL OF CRITICAL CARE MEDICINE
2015年
6期
549-552
,共4页
内皮特异性分子%脂多糖%肺损伤%炎症反应
內皮特異性分子%脂多糖%肺損傷%炎癥反應
내피특이성분자%지다당%폐손상%염증반응
Endocan%Lipopolysaccharide%Lung injury%Inflammatory response
目的:探讨内皮细胞特异性分子与炎症因子在脂多糖( LPS)导致的小鼠急性肺损伤( ALI)中的表达水平变化,及其与ALI的关系。方法复制LPS导致的小鼠ALI模型,将小鼠分为对照组与模型组(按时间点分别分为0、6、12和24 h)。模型组给予尾静脉注射内毒素(5 mg/kg),正常组在相同时间点给予尾静脉注射等量的磷酸缓冲盐溶液( PBS),在各个时间点麻醉取血后处死,取肺脏标本,观察肺脏病理形态学变化,测定肺脏的湿/干质量比与髓过氧化物酶( MPO),酶联免疫试剂盒测定炎症因子包括肿瘤坏死因子-α( TNF-α)、白细胞介素-6( IL-6)、高迁移率族蛋白1(HMGB1)与内皮特异性分子的表达,免疫印迹法观察核转录因子-κB ( NF-κB)与磷酸化NF-κB的变化。结果与对照组比较,模型组的肺组织损伤严重,肺湿/干质量比明显增加,MPO与炎症因子TNF-α、IL-6、HMGB1表达明显升高,同时内皮特异性分子与磷酸化NF-κB表达也明显升高。结论内皮特异性分子与炎症相关因子的表达变化可能提示LPS导致的小鼠ALI的进展,为早期干预ALI、降低多器官功能失调的发生率提供有益的参考。
目的:探討內皮細胞特異性分子與炎癥因子在脂多糖( LPS)導緻的小鼠急性肺損傷( ALI)中的錶達水平變化,及其與ALI的關繫。方法複製LPS導緻的小鼠ALI模型,將小鼠分為對照組與模型組(按時間點分彆分為0、6、12和24 h)。模型組給予尾靜脈註射內毒素(5 mg/kg),正常組在相同時間點給予尾靜脈註射等量的燐痠緩遲鹽溶液( PBS),在各箇時間點痳醉取血後處死,取肺髒標本,觀察肺髒病理形態學變化,測定肺髒的濕/榦質量比與髓過氧化物酶( MPO),酶聯免疫試劑盒測定炎癥因子包括腫瘤壞死因子-α( TNF-α)、白細胞介素-6( IL-6)、高遷移率族蛋白1(HMGB1)與內皮特異性分子的錶達,免疫印跡法觀察覈轉錄因子-κB ( NF-κB)與燐痠化NF-κB的變化。結果與對照組比較,模型組的肺組織損傷嚴重,肺濕/榦質量比明顯增加,MPO與炎癥因子TNF-α、IL-6、HMGB1錶達明顯升高,同時內皮特異性分子與燐痠化NF-κB錶達也明顯升高。結論內皮特異性分子與炎癥相關因子的錶達變化可能提示LPS導緻的小鼠ALI的進展,為早期榦預ALI、降低多器官功能失調的髮生率提供有益的參攷。
목적:탐토내피세포특이성분자여염증인자재지다당( LPS)도치적소서급성폐손상( ALI)중적표체수평변화,급기여ALI적관계。방법복제LPS도치적소서ALI모형,장소서분위대조조여모형조(안시간점분별분위0、6、12화24 h)。모형조급여미정맥주사내독소(5 mg/kg),정상조재상동시간점급여미정맥주사등량적린산완충염용액( PBS),재각개시간점마취취혈후처사,취폐장표본,관찰폐장병리형태학변화,측정폐장적습/간질량비여수과양화물매( MPO),매련면역시제합측정염증인자포괄종류배사인자-α( TNF-α)、백세포개소-6( IL-6)、고천이솔족단백1(HMGB1)여내피특이성분자적표체,면역인적법관찰핵전록인자-κB ( NF-κB)여린산화NF-κB적변화。결과여대조조비교,모형조적폐조직손상엄중,폐습/간질량비명현증가,MPO여염증인자TNF-α、IL-6、HMGB1표체명현승고,동시내피특이성분자여린산화NF-κB표체야명현승고。결론내피특이성분자여염증상관인자적표체변화가능제시LPS도치적소서ALI적진전,위조기간예ALI、강저다기관공능실조적발생솔제공유익적삼고。
Objective To explore endocan and inflammatory factors expression during lipopolysaccharide ( LPS) induced acute lung injury ( ALI ) in mice, and to explore their roles during ALI in mice.Methods LPS-induced mice ALI models were assigned into control groups and LPS groups (0, 6, 12, and 24 h according to time points pre-scheduled).The ALI models were injected with 5 mg/kg LPS through tail vein, and the normal control groups were administrated with equal volume phosphate buffer solution (PBS). Mice were anesthetized, and blood samples were collected.Mice were then killed; lungs were obtained to perform next experiments.Lung samples were processed and hemotoxylin and eosin staining ( HE ) were done to examine the histopathological changes. Myeloperoxidase ( MPO) and wet to dry of lungs were measured.Levels in mice serum of tumor necrosis factorα( TNF-α) , interlukin -6 ( IL -6 ) , high mobility group box1 ( HMGB1 ) were analyzed. Expression of nuclear factor-κB ( NF-κB) and phosphorylated nuclear factor-κB were tested by immunoblotting assays.Results Compared with the control groups, LPS administration resulted in severe lung injury, increased lung wet/dry ratio.MPO levels, expression of TNF -α, IL -6, and HMGB1were elevated significantly after LPS treatment.Meantime, LPS also increased endocan and phosphorylated NF -κB expression in mice.Conclusion The expression changes of inflammatory factors and endocan may suggest the development process during LPS induced lung injury.The present study may offer beneficial reference for treating ALI, and decreasing multiple organs failure ( MOF) in earlier phase clinically.