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作 者:宁杰[1] 姜玉禄 李俞锦[1] 李艳华[1] 庞庆丰[2]
机构地区:[1]云南省第一人民医院麻醉科,云南昆明650032 [2]江南大学无锡医学院病理生理学教研室,江苏无锡214122
出 处:《昆明理工大学学报(自然科学版)》2013年第6期84-88,101,共6页Journal of Kunming University of Science and Technology(Natural Science)
基 金:国家自然科学基金资助项目(81270126)
摘 要:研究乳铁蛋白(lactoferrin,LF)对脂多糖诱导的急性肺损伤(acute lung injury,ALI)的保护作用,并探讨其可能机制.清洁级雄性昆明小鼠腹腔注射LPS 5 mg/kg前1h或注射LPS后1h给予LF 5 mg/body,同时以2mg/kg地塞米松治疗组为阳性对照组.给予LPS 12h后,收集左肺肺泡灌洗液.检测白细胞介素-10及肿瘤坏死因子-α的含量、总蛋白含量;离心后将沉淀重悬检测灌洗液中总细胞数.取右肺上叶速冻于-80℃冰箱,检测肺组织中髓过氧化物酶含量;中叶称湿、干重,计算肺湿/干重比;下叶进行HE染色,观察肺组织病理学改变.结果发现,LF能明显减轻肺泡腔出血、水肿、炎细胞浸润等病理过程,肺组织病理学评分明显降低(P<0.05);LF能降低肺组织MPO活性、肺泡灌洗液中总细胞、总蛋白含量、W/D和TNF-α含量(P<0.05);增加肺组织IL-10含量(P<0.05).这些结果说明,LF对LPS诱导的急性肺损伤有显著的预防和治疗作用.This study aims to investigate the protective effect and mechanisms of lactoferrin (LF) on acute lung injury (ALI) induced by lipopolysaceharide (LPS). Kunming male mice of clean grade are given LF ( 5 mg/ body) by intraperitoneal injection of 5 mg/kg LPS at 1 h before or after LPS administration. In the meanwhile, the positive control group is injected 2 mg/kg. 12 hours after LPS administration, the bronchoalveolar lavage flu- id of the left lung are collected to test the content of TNF - α, IL - 10, the concentration of protein and the sedi- mentary cells. The right lung is harvested for histology and determination of the myeloperoxidase activity and W/ D. The results show that LF significantly attenuates the scores of the lung tissues, myeloperoxidase activity, the total cells, the total protein concentration, W/D and the content of TNF - α( P 〈 0. 05 ), while increasing the content of IL - 10 ( P 〈 0. 05 ). These results suggest that LF could inhibit the inflammatory reaction of the mice with LPS- induced ALl.
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