Akademik Veri Yönetim Sistemi
MEDIATORS OF INFLAMMATION, cilt.2016, 2016 (SCI-Expanded)
Background. Inflammation and oxidative stress (OxS) contribute to the pathogenesis of diabetic kidney disease (DKD) and contrastinduced nephropathy (CIN). Patients with DKD were found to be more prone to CIN. Interleukin-33 (IL-33) is a proinflammatory cytokine, but its role in DKDand CINis unknown. Methods. Thirty male Sprague-Dawley rats were enrolled. The first group was comprised of healthy rats (HRs), whereas the other four groups were made up of diabetic rats (DRs), diabetic rats with contrastinduced nephropathy (CIN + DRs), melatonin-treated diabetic rats (MTDRs), andmelatonin-treated CIN + DRs (MTCIN + DRs). All groups except the HRs received 50mg/kg/day streptozotocin (STZ). CIN + DRs were constituted by administrating 1.5mg/kg of intravenous radiocontrast dye on the 35th day. MTDRs andMTCIN + DRs were given 20mg/kg/day of intraperitoneal injection of melatonin (MT) from the 28th day for the constitutive seven days. Results. We observed increased IL-33 in the kidney tissue following induction of CIN in DRs. To determine whether MT is effective in preventing CIN, we administered MT in CIN + DRs and demonstrated that kidney tissue levels of OxS markers, inflammatory cytokines, and IL-33 were significantly diminished in MTCIN + DRs compared with other groups without MT treatment (p < 0.05). Conclusion. Inhibition of IL-33 with MT provides therapeutic potential in DKD with CIN.