肺组织细胞自噬在内毒素诱导的急性肺损伤中发挥保护作用
投稿时间:2015-07-24  修订日期:2015-08-19  点此下载全文
引用本文:郜冶,王妮,张锦.肺组织细胞自噬在内毒素诱导的急性肺损伤中发挥保护作用[J].医学研究杂志,2016,45(4):90-94
DOI: 10.11969/j.issn.1673-548X.2016.04.024
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作者单位E-mail
郜冶 110004 沈阳, 中国医科大学盛京医院麻醉科  
王妮 110004 沈阳, 中国医科大学盛京医院麻醉科  
张锦 110004 沈阳, 中国医科大学盛京医院麻醉科 zhangj_sj@163.com 
基金项目:沈阳市科技计划项目(F14-231-1-60)
中文摘要:目的 探讨在内毒素(lipopolysaccharide, LPS)诱导的急性肺损伤(acute lung injury, ALI)中肺组织细胞自噬是否发挥保护作用。方法 24只小鼠随机分为3组,每组8只。对照组(C):腹腔注射生理盐水;LPS组(L):腹腔注射LPS(30mg/kg);LPS+自噬拮抗剂组(L+3MA):在注射LPS前30min,腹腔注射3-MA(15mg/kg)。结果 肺组织细胞自噬被抑制后(p62水平增高,LC3Ⅱ/Ⅰ水平及电镜每高倍镜视野的自噬小均数下降,差异有统计学意义(P<0.05)),肺损伤加重,即TNF-α、IL-6、肺泡灌洗液中总蛋白及肺泡灌洗液中IgM浓度明显升高,差异有统计学意(P<0.05)。结论 肺组织细胞自噬在内毒素诱导的急性肺损伤中发挥保护作用。
中文关键词:内毒素  急性肺损伤  自噬  3-甲基腺嘌呤
 
Autophagy of the Lung Tissue Cells Play a Protective Role in Lipopolysaccharide-induced Acute Lung Injury in Rat
Abstract:Objective To investigate the effect of autophagy of the lung tissue cells on lipopolysaccharide(LPS)-induced acute lung injury (ALI)in rat. Methods Twenty-four male C57BL/6 rats were randomly assigned to three groups, the control(C), LPS(L) and LPS+3-MA (methyladenine) (L+3MA) groups. The three groups received different treatment, then light microscope and electronic microscopy were used to evaluate the degree of lung injury and the level of autophagy. The enzyme-linked immunosorbent assay (ELISA) was used to detected tumor necrosis factor alpha (TNF-α), interleukin-6(IL-6), the total protein of bronchoalveolar lavage fluid(BAL) and the concentration of IgM in BAL. The western blot was used to measure LC3Ⅱ/Ⅰand P62 in lung tissue. Results In the L+3MA group, TNF-α, IL-6, total protein of BAL and the concentration of IgM in BAL were increased(P<0.05) compared to the L group. In the L group, the level of LC3Ⅱ/Ⅰand the number of autophagosome in every high magnification field increased, but the level of p62 declined, compared to the L+3MA group. Conclusion Autophagy of the lung tissue cells play a protective role in lipopolysaccharide-induced acute lung injury in rat.
keywords:Lipopolysaccharide  Acute lung injury  Autophagy  3-Methyladenine
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