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地塞米松对脂多糖诱导的急性肺损伤幼鼠肺表面活性物质蛋白-D的影响
引用本文:舒林华,薛辛东,舒林宏,刘春峰,韩晓华,吴红敏,尚云晓,蔡栩栩,魏克伦.地塞米松对脂多糖诱导的急性肺损伤幼鼠肺表面活性物质蛋白-D的影响[J].中国当代儿科杂志,2007,9(2):155-158.
作者姓名:舒林华  薛辛东  舒林宏  刘春峰  韩晓华  吴红敏  尚云晓  蔡栩栩  魏克伦
作者单位:舒林华,薛辛东, 舒林宏,刘春峰,韩晓华,吴红敏,尚云晓, 蔡栩栩, 魏克伦
摘    要:目的:肺表面活性物质蛋白D(SP-D)被认为是急性肺损伤(ALI)和急性呼吸窘迫综合征(ARDS)有价值的生物指标。该研究旨在探讨幼鼠ALI时及地塞米松干预后肺组织SP-D的变化。方法:144只SD大鼠被随机分为正常对照组、肺损伤组和地塞米松治疗组。腹腔内注射脂多糖(LPS,4 mg/kg)建立急性肺损伤模型, 正常对照组注射等量生理盐水, 治疗组于注射LPS 1小时后注射地塞米松(5 mg/kg)。LPS注射后6,12,24,36,48,72 h 每组各处死8只大鼠。用Western blot方法测定肺组织SP-D的相对含量。结果:与正常对照组相比,ALI组在注射LPS后36,48,72 h SP-D含量明显下降(P<0.01),在48 hrs达最低点(0.92±0.11 vs 3.27±0.52)。地塞米松治疗组于注射LPS后36,48,72 h SP-D含量明显高于ALI组 (P<0.01), 6,12,24,36和48 h 与对照组相比差异无显著性, 72 h差异有显著性(P<0.05)。结论:急性肺损伤早期幼鼠肺组织SP-D含量降低。早期应用地塞米松能使ALI肺组织下降的SP-D明显上升。[中国当代儿科杂志,2007,9(2):155-158]

关 键 词:脂多糖  急性肺损伤  肺表面活性蛋白D  地塞米松  大鼠  
文章编号:1008-8830(2007)02-0155-04
收稿时间:2006-10-31
修稿时间:2006-12-15

Effect of dexamethasone on the content of pulmonary surfactant protein D in young rats with acute lung injury induced
SHU Lin-Hu,XUE Xin-Dong,SHU Lin-Hong,LIU Chun-Feng,HAN Xiao-Hu,WU Hong-Min,SHANG Yun-Xiao,CAI Xu-Xu,WEI Ke-Lun.Effect of dexamethasone on the content of pulmonary surfactant protein D in young rats with acute lung injury induced[J].Chinese Journal of Contemporary Pediatrics,2007,9(2):155-158.
Authors:SHU Lin-Hu  XUE Xin-Dong  SHU Lin-Hong  LIU Chun-Feng  HAN Xiao-Hu  WU Hong-Min  SHANG Yun-Xiao  CAI Xu-Xu  WEI Ke-Lun
Institution:SHU Lin-Hua, XUE Xin-Dong, SHU Lin-Hong, LIU Chun-Feng, HAN Xiao-Hua, WU Hong-Min, SHANG Yun-Xiao, CAI Xu-Xu, WEI Ke-Lun
Abstract:OBJECTIVE: Pulmonary surfactant protein-D (SP-D) is regarded as a valuable biomarker in acute lung injury (ALI) and acute respiratory distress syndrome (ARDS). This study was to explore the changes of SP-D content in lung tissue following ALI and the effect of dexamethasone (Dex) on the SP-D content in young rats. METHODS: One hundred and forty-four 21-day-old Sprague-Dawley rats were randomly assigned into control, ALI and Dex-treated groups. ALI was induced by intraperitoneal injection of lipopolysaccharide (LPS) (4 mg/kg) in the rats from the ALI and Dex-treated groups. Normal saline was given for the control group. Dex (5 mg/kg) was administered 1 hr after LPS injection in the Dex-treated group. At each time interval of 6, 12, 24, 36, 48 and 72 hrs after LPS injection, eight rats of each group were randomly chosen and sacrificed. Western blot was employed to detect the content of SP-D in lung tissues. RESULTS: The pulmonary SP-D content decreased significantly at 36, 48 and 72 hrs after LPS administration in the ALI group, and reduced to a nadir (0.92 +/-0.11 vs 3.27 +/- 0.52) at 48 hrs compared with that of the control group (P < 0.01). The SP-D content in the Dex-treated group increased significantly at 36,48 and 72 hrs after LPS administration when compared with the ALI group (P < 0.01). A significant difference in the SP-D content between the Dex-treated and the control group was noted only at 72 hrs after LPS administration (P < 0.05). CONCLUSIONS: The SP-D content in lung tissue was reduced following ALI in young rats at the early stage. Early administration of Dex can significantly increase the pulmonary SP-D content.
Keywords:Lipopolysaccharide  Acute lung injury  Pulmonary surfactant protein D  Dexamethasone  Rats
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