The pathophysiology mechanisms of anxiety disorders are closely associated with neuroinflammation mediated by the nucleotide-binding oligomerization domain-like receptor protein 3（ NLRP3） inflammasome. Research indicates that NLRP3 inflammasomes activate via classical and non-classical pathways under stress or environmental stimuli， releasing proinflammatory factors such as interleukin-1β（ IL-1β） and interleukin-18（ IL-18）， leading to impaired synaptic plasticity in the hippocampus and prefrontal cortex， as well as neuronal pyroptosis， ultimately inducing anxiety-like behaviors. Its regulatory network exhibits multidimensional characteristics： brain region specificity， environment-gene interactions， gut-brain axis， and epigenetic mechanisms. In terms of targeted interventions， drugs and natural ingredients exert therapeutic effects by inhibiting NLRP3 inflammasome assembly， modulating microglial phenotypic polarization， and activating antioxidant pathways. Future research should focus on brain region regulatory heterogeneity， mechanisms of neuronal subpopulation interactions， and the development of efficient small-molecule inhibitors. This paper systematically analyzes the multidimensional regulatory network of the NLRP3 inflammasome， aiming to provide a theoretical basis for mechanistic interventions in anxiety disorders.