regulates MSU-induced apoptosis and inflammatory response through TLR4/MyD88/NF-κB signaling pathway.

The increased inflammation associated with interleukin-1α () induced by monosodium urate (MSU) crystal-induced gouty arthritis is mediated through the NLRP3 inflammasome and NF-κB signaling pathways. This study investigated the role of in MSU-mediated inflammation and its therapeutic potential. MSU crystals were applied to THP-1 macrophages and human vascular endothelial cells (HUVECs) with or without knockdown. Quantitative reverse transcription polymerase chain reaction (qRT-PCR), western blotting (WB), cell counting kit-8 (CCK-8), flow cytometry, and enzyme-linked immunosorbent assay (ELISA) were used to assess expression, cell viability, apoptosis, and the generation of inflammatory cytokines. The activation of the NLRP3 inflammasome and TLR4/MyD88/NF-κB pathways was evaluated, with TAK-242 used to assess synergistic effects. MSU increased expression, induced apoptosis, and reduced cell viability in HUVECs, effects reversed by knockdown. knockdown media mitigated apoptosis in HUVECs exposed to conditioned media from MSU-stimulated THP-1 macrophages. knockdown reduced MSU-induced proinflammatory cytokines and NLRP3 activation in THP-1 cells. TAK-242 showed synergistic effects, while knockdown inhibited TLR4/MyD88/NF-κB activation. promotes cell death and inflammation in MSU-induced gout. Knockdown of mitigates these effects, suggesting it may be a potential therapeutic target for MSU-induced inflammation.