首页|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

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目的:探讨七氟醚通过调控p38/MAPK信号通路对脂多糖(LPS)诱导的肺泡巨噬细胞M1型极化的影响.方法:采用1 μg/ml的LPS刺激RAW264.7细胞24 h,暴露于不同浓度(1%、2%、4%)七氟醚后,分别采用MTT、ELISA、RT-qPCR及Western blot检测细胞活力、炎症相关因子及相关通路蛋白的表达情况.结果:LPS刺激使RAW264.7细胞活力降低,M1型促炎症因子的表达升高,M2型抗炎症因子的表达降低,p38/MAPK磷酸化蛋白的表达水平升高(P<0.05).七氟醚处理后,细胞活力明显增强,抗炎因子水平明显上升,促炎因子水平显著下降,p38蛋白的磷酸化水平降低,且与七氟醚浓度具有依赖性(P<0.05).p38/MAPK抑制剂SB202190加剧了七氟醚对肺泡巨噬细胞M1型极化的抑制作用.结论:七氟醚能够抑制LPS诱导的肺泡巨噬细胞M1型极化,可能是通过调节p38/MAPK信号通路实现的.
Sevoflurane inhibits M1-type polarization of alveolar macrophages induced by lipopolysaccharide through p38/MAPK signaling pathway
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.

SevofluraneLPSMacrophageInflammatory cytokines

王领、赵雪、王金林

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武汉市第八医院麻醉科,武汉 430000

湖北省中西医结合医院急诊医学科,武汉 430000

七氟醚 脂多糖 巨噬细胞 炎症因子

2024

中国免疫学杂志
中国免疫学会,吉林省医学期刊社

中国免疫学杂志

CSTPCD北大核心
影响因子:0.926
ISSN:1000-484X
年,卷(期):2024.40(9)