Chloroquine regulates the lipopolysaccharide-induced inflammatory response in RAW264.7 cells.
Allergol Immunopathol (Madr)
; 52(4): 97-103, 2024.
Article
em En
| MEDLINE
| ID: mdl-38970272
ABSTRACT
INTRODUCTION AND OBJECTIVES:
Macrophage-induced inflammation plays a key role in defense against injury and harmful pathogens. Autophagy and the inflammatory response are associated; however, the relationship between the autophagy pathway and lipopolysaccharide (LPS)- induced inflammatory responses remains unknown. We aimed to determine the effect of autophagy on the LPS-induced myeloid differentiation factor 88 (MyD88)/nuclear transcription factor kB (NF-kB) pathway-mediated inflammatory response in RAW264.7 cells. MATERIALS ANDMETHODS:
To determine the effect of autophagy on the LPS-induced inflammatory response, using various in vitro assays, we determined the effect of autophagy inhibitors and inducers on the inflammatory response in RAW264.7 cells.RESULTS:
Chloroquine (CQ), an autophagy inhibitor, suppressed pro-inflammatory cytokines, including interleukin (IL)-1ß, IL-6, and tumor necrosis factor α (TNFα) in LPS-stimulated RAW264.7 cells. CQ also affected inflammatory mediators such as myeloid differentiation factor 88 and NF-kB in LPS-stimulated RAW264.7 cells.CONCLUSION:
This study demonstrated that CQ regulates the LPS-induced inflammatory response in RAW264.7 cells. We propose that targeting the regulation of pro-inflammatory cytokine levels and inflammatory mediators using CQ is a promising therapeutic approach for preventing inflammatory injury. CQ serves as a potential therapeutic target for treating various inflammatory diseases.Palavras-chave
Texto completo:
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Base de dados:
MEDLINE
Assunto principal:
Cloroquina
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Lipopolissacarídeos
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Citocinas
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NF-kappa B
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Fator 88 de Diferenciação Mieloide
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Macrófagos
Limite:
Animals
Idioma:
En
Ano de publicação:
2024
Tipo de documento:
Article