Chronic low-grade inflammation is a well-recognized feature of type 2 diabetes mellitus (T2DM), contributing significantly to the development of insulin resistance and the progression of diabetes-related complications. Elevated levels of inflammatory cytokines and immune mediators have been closely linked to impaired insulin signaling and β-cell dysfunction. Consequently, targeting inflammation has emerged as a promising strategy in the management of diabetes. Among antidiabetic agents, glucagon-like peptide-1 (GLP-1) receptor agonists, particularly semaglutide, have gained attention not only for their glucose-lowering efficacy but also for their potential anti-inflammatory properties. 

Semaglutide, a long-acting GLP-1 analogue, has demonstrated significant benefits in improving glycemic control, reducing body weight, and providing cardiovascular protection in patients with T2DM. Beyond these metabolic effects, emerging evidence highlights the anti-inflammatory potential of semaglutide. Preclinical and clinical studies have suggested that semaglutide can modulate inflammatory pathways, attenuate oxidative stress, and reduce circulating levels of pro-inflammatory cytokines such as TNF-α, IL-6, and CRP. Moreover, semaglutide may exert direct protective effects on various organs, including the cardiovascular system, liver, kidneys, and adipose tissue, through its anti-inflammatory actions. 

Despite these promising findings, the precise molecular mechanisms underlying the anti-inflammatory effects of semaglutide remain incompletely understood. Several potential pathways have been proposed, including inhibition of NF-κB signaling, reduction of oxidative stress, modulation of immune cell activity, and improvement of mitochondrial function. Understanding these mechanisms may provide new insights into the broader therapeutic benefits of semaglutide, beyond glycemic control, and support its role as a valuable agent in the management of diabetes and its associated inflammatory complications.