{Reference Type}: Journal Article
{Title}: Chloroquine regulates the lipopolysaccharide-induced inflammatory response in RAW264.7 cells.
{Author}: Ota N;Endo S;Honma K;Iwayama K;Yamashita H;Tatsunami R;Sato K;
{Journal}: Allergol Immunopathol (Madr)
{Volume}: 52
{Issue}: 4
{Year}: 2024
{Factor}: 2.094
{DOI}: 10.15586/aei.v52i4.1083
{Abstract}: <B>OBJECTIVE: </B>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.<BR><B>METHODS: </B>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.<BR><B>RESULTS: </B>Chloroquine (CQ), an autophagy inhibitor, suppressed pro-inflammatory cytokines, including interleukin (IL)-1β, 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.<BR><B>CONCLUSIONS: </B>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.