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首页|期刊导航|中国免疫学杂志|七氟醚通过p38/MAPK信号通路抑制脂多糖诱导的肺泡巨噬细胞M1型极化

七氟醚通过p38/MAPK信号通路抑制脂多糖诱导的肺泡巨噬细胞M1型极化

王领 赵雪 王金林

中国免疫学杂志2024,Vol.40Issue(9):1850-1855,6.
中国免疫学杂志2024,Vol.40Issue(9):1850-1855,6.DOI:10.3969/j.issn.1000-484X.2024.09.010

七氟醚通过p38/MAPK信号通路抑制脂多糖诱导的肺泡巨噬细胞M1型极化

Sevoflurane inhibits M1-type polarization of alveolar macrophages induced by lipopolysaccharide through p38/MAPK signaling pathway

王领 1赵雪 1王金林2

作者信息

  • 1. 武汉市第八医院麻醉科,武汉 430000
  • 2. 湖北省中西医结合医院急诊医学科,武汉 430000
  • 折叠

摘要

Abstract

Objective:To investigate the effect of sevoflurane on M1 polarization of alveolar macrophages induced by lipopoly-saccharide(LPS)by regulating p38/MAPK signaling pathway.Methods:RAW264.7 cells were stimulated with 1 μg/ml LPS for 24 h and exposed to different concentrations(1%,2%,4%)of sevoflurane.After that,MTT,ELISA,RT-qPCR and Western blot assays were used to detect cell viability,inflammation factors and signaling pathway-related protein levels.Results:LPS stimulation led to de-creased cell viability and M2-type anti-inflammatory cytokine levels,and increased M1-type pro-inflammatory cytokine levels and phosphorylation of p38/MAPK in RAW264.7 cells(P<0.05).After sevoflurane treatment,the cell viability and anti-inflammatory cyto-kine levels were significantly enhanced,and the pro-inflammatory cytokine levels and phosphorylation of p38 were significantly de-creased in a concentration-dependent manner(P<0.05).The p38/MAPK inhibitor SB202190 intensified the inhibitory effect of sevoflu-rane on M1-type polarization of alveolar macrophages.Conclusion:Sevoflurane inhibits LPS-induced M1 polarization of alveolar mac-rophages,possibly by regulation of the p38/MAPK signaling pathway.

关键词

七氟醚/脂多糖/巨噬细胞/炎症因子

Key words

Sevoflurane/LPS/Macrophage/Inflammatory cytokines

分类

医药卫生

引用本文复制引用

王领,赵雪,王金林..七氟醚通过p38/MAPK信号通路抑制脂多糖诱导的肺泡巨噬细胞M1型极化[J].中国免疫学杂志,2024,40(9):1850-1855,6.

中国免疫学杂志

OA北大核心CSTPCD

1000-484X

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