The nuclear factor-κB (NF-κB) pathway involves numerous transcription factors such as IL-1β, IL-6, tumor necrosis factor-α (TNF-α), and monocyte chemotactic protein 1 (MCP-1), which are increased in pelvic inflammatory disease [76]; it was reported that AA inhibits the activation of the NF-κB pathway and also of the nucleotide-binding domain-like receptor protein 3 (NLRP3) inflammasome, which mediates the release and maturation of IL-1β, thus significantly reducing the concentration of inflammatory cytokines and chemokines and ameliorating oxidative stress. Here, CCL2 is linked to pelvic inflammatory disease.