Synergistic Effects of IL-16 and KRAS in Endometriosis with Emphasis on Oxidative Stress

Background & Objective: Endometriosis is characterized by the growth of endometrial-like tissue outside the uterus, leading to inflammation, pain, and infertility. Its pathogenesis involves genetic, immunological, and hormonal factors. This study examines the synergistic roles of IL‑16 and KRAS gene expression in endometriosis and their interaction with oxidative stress markers to identify potential biomarkers for targeted therapy.Materials & Methods: A case-control study was conducted with 300 subjects, including 150 cases diagnosed with endometriosis and 150 healthy controls. Gene expression levels of IL‑16 and KRAS were analyzed using real-time PCR. Oxidative stress markers, including Superoxide Dismutase (SOD), glutathione peroxidase, and vitamin C, along with the inflammatory cytokine IL‑6, were measured.Results: IL‑16 and KRAS gene expression levels were significantly elevated in cases compared with controls, with KRAS identified as an independent predictor (P=0.002). Oxidative stress markers demonstrated a marked reduction in SOD and glutathione peroxidase levels, accompanied by decreased vitamin C levels. Elevated IL‑6 levels (>5.57 pg/mL, OR=7.91, P=0.032) were associated with increased inflammation and oxidative stress related cellular damage.Conclusion: The findings indicate that IL‑16 and KRAS contribute to the progression of endometriosis through oxidative stress-mediated genetic alterations and inflammatory pathways. The study underscores the combined impact of oxidative imbalance, IL‑6 driven inflammation, and KRAS dysregulation in disease pathogenesis. Unlike previous research focusing on genetic polymorphisms, this study provides novel insights into gene expression patterns and their clinical implications. Further investigation into the mechanistic interactions among IL‑16, KRAS, and oxidative stress may aid in the development of targeted therapeutic strategies.