Sweeney, GaryZhang, Bojun2025-11-112025-11-112025-07-282025-11-11https://hdl.handle.net/10315/43297Chronic inflammation, driven by fa tors such as iron overload, contributes to metabolic, cardiovascular, and degenerative diseases. Excess iron promotes pro-inflammatory cytokines release and increased production of reactive oxygen species (ROS) in macrophages via transcription factors, such as IRF and NF-κB. This study investigated whether ALY688, an adiponectin receptor agonist, mitigate iron-induced inflammation. Using ferrous sulfate (FeSO₄) treated RAW 264.7 macrophages, I found that ALY688 markedly reduced the activation of both NF-κB and IRF pathways, suppressed ROS levels, and reversed the expression of inflammatory and antioxidant genes. Iron overload significantly upregulated pro-inflammatory cytokines (IL-1β, TNF-α, IL-6) and oxidative stress-related genes (NOX2), while downregulating anti-inflammatory mediators such as IL-10. Together, these findings support a regulatory role of ALY688 in attenuating iron-induced oxidative stress and inflammation in macrophages, suggesting that ALY688 may serve as a promising therapeutic candidate for iron overload-associated inflammatory disorders.Author owns copyright, except where explicitly noted. Please contact the author directly with licensing requests.BiologyMolecular biologyElectronic Thesis or Dissertation2025-11-11Iron overloadAnti-inflammationAdiponectin receptor agonistMacrophage activation