When UA exceeds its physiological antioxidant threshold, it may induce pathological damage through multiple mechanisms: (1) overproduction of ROS via the mitochondrial respiratory chain and NADPH oxidases (NOXs) (32);(2) activation of the NF-κB pathway, resulting in upregulation of pro-inflammatory cytokines (33);(3) assembly of the NLRP3 inflammasome, triggering IL-1β-mediated inflammatory responses (34, 35);and (4) inhibition of cerebral endothelial nitric oxide synthase, reducing hippocampal perfusion and disrupting depression-related neural circuits (36). Here, IL1B is linked to depressive symptom measurement.