Sevoflurane inhibits M1-type polarization of alveolar macrophages induced by lipopolysaccharide through p38/MAPK signaling pathway
10.3969/j.issn.1000-484X.2024.09.010
- VernacularTitle: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
- Author:
Ling WANG
1
;
Xue ZHAO
;
Jinlin WANG
Author Information
1. 武汉市第八医院麻醉科,武汉 430000
- Keywords:
Sevoflurane;
LPS;
Macrophage;
Inflammatory cytokines
- From:
Chinese Journal of Immunology
2024;40(9):1850-1855
- CountryChina
- Language:Chinese
-
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.
