Role of excessive autophagy in the regulation of interleukin-1β in inflammatory effect of acute respiratory distress syndrome

Wang Chuanjiang; Xu Fang

doi:10.13406/j.cnki.cyxb.001144

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Role of excessive autophagy in the regulation of interleukin-1β in inflammatory effect of acute respiratory distress syndrome

更新时间：2024-01-17

- Role of excessive autophagy in the regulation of interleukin-1β in inflammatory effect of acute respiratory distress syndrome
- Journal of Chongqing Medical University Vol. 42, Issue 1, Pages: 15-20(2017)
- 作者机构：
  
  重庆医科大学附属第一医院急诊医学科&重症医学科
- 作者简介：
- 基金信息：
- DOI：10.13406/j.cnki.cyxb.001144
  CLC： R563.8
- Published：2017，
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[1]王川江,徐昉.过度自噬对白介素-1β在急性呼吸窘迫综合征中失控性炎症的调节作用研究[J].重庆医科大学学报,2017,42(01):15-20.

Wang Chuanjiang, Xu Fang. Role of excessive autophagy in the regulation of interleukin-1β in inflammatory effect of acute respiratory distress syndrome. [J]. Journal of Chongqing Medical University 42(1):15-20(2017)
[1]王川江,徐昉.过度自噬对白介素-1β在急性呼吸窘迫综合征中失控性炎症的调节作用研究[J].重庆医科大学学报,2017,42(01):15-20. DOI： 10.13406/j.cnki.cyxb.001144.

Wang Chuanjiang, Xu Fang. Role of excessive autophagy in the regulation of interleukin-1β in inflammatory effect of acute respiratory distress syndrome. [J]. Journal of Chongqing Medical University 42(1):15-20(2017) DOI： 10.13406/j.cnki.cyxb.001144.

摘要

目的:探究白介素-1β（interleukin-1β

IL-1β）在急性呼吸窘迫综合征（acute respiratory distress syndrome

ARDS）中的表达以及通过自噬调节IL-1β在ARDS中的作用。方法:将小鼠分为脂多糖（lipopolysaccharide

LPS）模型组、LPS+3-甲基腺嘌呤（3-methyladenine

3-MA）干预组和LPS+PBS对照组

每组随机分配5只C57BL/6雄性小鼠

通过ELISA检测小鼠血清、肺泡灌洗液中IL-1β的表达

RT-PCR对小鼠肺组织中IL-1β进行定量分析

Western blot检测LPS诱导的ARDS小鼠肺组织中微管相关蛋白LC3（LC3Ⅱ/LC3Ⅰ）以及P62表达

使用3-MA干预ARDS小鼠模型

后检测IL-1β、肿瘤坏死因子-α（tumor necrosis factor-α

TNF-α）、白介素-6（interleukin-6

IL-6）、γ-干扰素（interferon-γ

IFN-γ）等细胞因子以及自噬水平变化。结果:1LPS诱导ARDS小鼠模型中

IL-1β在外周血、肺泡灌洗液以及肺组织中的表达较正常对照组明显升高（P值分别为0.000、0.000、0.021）

Western blot检测P62蛋白逐步降低（F=14.376

P=0.005）

LC3Ⅱ/LC3Ⅰ值逐步升高（F=53.799

P=0.000）;23-MA处理ARDS小鼠模型后

IL-1β以及TNF-α、IL-6、IFN-γ等细胞因子在外周血、肺泡灌洗液以及肺组织中的表达较对照组和模型组明显降低（P<0.01）

Western blot检测P62蛋白逐步降低（F=20.037

P=0.002）

LC3Ⅰ/LC3Ⅱ值逐步升高（F=38.726

P=0.000）。结论:抑制过度自噬可降低IL-1β水平

减弱IL-1β的促炎作用

调控ARDS的失控性炎症效应。

Abstract

Objective:To explore the expression of the interleukin-1β(IL-1β)in severe acute respiratory distress syndrome(ARDS)and the regulation of IL-1βby autophagy in ARDS. Methods:Mice were divided into lipopolysaccharide(LPS)induced ARDS model group

LPS+3-methyladenine(3-MA)autophagy inhibition intervention group and LPS+PBS control group;each group were randomly assigned 5 C57BL/6 male mice. The expressions of IL-1βin serum and bronchoalveolar lavage fluid were detected by ELISA. Quantitative analysis of IL-1βin the lung tissue of mice was conducted by RT-PCR. Expressions of LPS induced blot related protein LC3(LC3II/LC3I)and the P62 were detected by Western blot. 3-MA was used to intervene ARDS mouse model

and changes in expressions of tumor necrosis factor-α(TNF-α)

interleukin-6(IL-6)

interferon-γ(IFN-γ)and other cytokines and autophagy levels were detected. Results:1In LPS induced ARDS mice model

the expressions of IL-1βin lung tissue and lavage fluid was obviously higher than those of normal control group in peripheral blood and bronchoalveolar lavage(P=0.000

P=0.000

P=0.021). P62 protein detected by Western blot(F=14.376

P=0.005)was decreased gradually; the ratio of LC3 was increased gradually(LC3Ⅱ/LC3Ⅰ F=53.799

P=0.000). 2In 3-MA mouse model of ARDS

IL-1β

TNF-α

IL-6

IFN-γ and cytokine expressions in lung tissue and lavage fluid were significantly lower than those of control group and model group in the peripheral blood and bronchoalveolar lavage(P<0.01). Western blot detection of P62 protein was decreased gradually(F =20.037

P =0.002)

the ratio of LC3 Ⅰ/LC3 Ⅱ was increased gradually(F=38.726

P=0.000). Conclusion:Inhibiting excessive autophagy can decrease the level of IL-1β and reduce the proinflammatory effect of IL-1β

thus controlling the inflammatory effect of ARDS.

关键词

白介素-1β急性呼吸窘迫综合征自噬

Keywords

interleukin-1 betaacute respiratory distress syndromeautophagy

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