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Ig M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。
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.
出处
《医学研究杂志》
2016年第4期90-94,共5页
Journal of Medical Research
基金
沈阳市科技计划项目(F14-231-1-60)
关键词
内毒素
急性肺损伤
自噬3-甲基腺嘌呤
Lipopolysaccharide
Acute lung injury
Autophagy
3 - Methyladenine
