Furthermore, baicalein regulated the expression of surface markers CD86 and CD206, thereby inhibiting M1 polarization and promoting the transition from an M1 to an M2 phenotype.<h4>Conclusion</h4>This study demonstrates that baicalein improves the inflammatory microenvironment of gouty arthritis through multi-target and multi-pathway synergistic effects, including the inhibition of oxidative stress, immune regulation, and modulation of key signaling pathways. Here, CD86 is linked to gout.