Diabetic nephropathy (DN) is a serious complication of diabetes mellitus. Moreover,it is amongst the most common causes of end-stage renal failure. Inflammation is a crucial player in both development and progression of DN. JAK2/STA3 is a pleotropic cascade reported to regulate diverse inflammatory events. Previous studies reported involvement of JAK2/STA3 signal transduction pathway in diabetes-associated renal injury. In the current study, the inhibitory effect of nifuroxazide (25 mg/kg/day, orally) against inflammatory condition associating diabetic kidney progression in rats was evaluated. The underlying hypothesis is mainly via the inhibitory effect of nifuroxazide on STAT3 signaling. Results revealed that nifuroxazide effectively inhibited STAT3 activation in diabetic male rats, improved glomerular filtration function, protected against diabetes-induced histopathological and ultramicroscopic structural alterations. Further, nifuroxazide treatment significantly reduced renal macrophage infiltration and fibrosis and decreased mRNA and protein levels of TNF-α and IL-18 in diabetic renal tissue. The current findings shed the light on nifuroxazide's efficacy as an alternative anti-inflammatory therapy to hinder the development and progression of DN in diabetic patients mainly via STAT3 inhibition.

糖尿病肾病（DN）是糖尿病的严重并发症。此外，它是终末期肾衰竭的最常见原因之一。炎症是DN发生和发展的关键因素。JAK2 / STA3是据报道可调节多种炎症事件的多效性级联反应。先前的研究报道了JAK2 / STA3信号转导通路与糖尿病相关的肾损伤有关。在当前的研究中，评估了尼呋拉嗪（25 mg / kg /天，口服）对与大鼠糖尿病性肾病相关的炎性疾病的抑制作用。潜在的假设主要是通过尼呋拉嗪对STAT3信号的抑制作用。结果显示，尼呋沙嗪可有效抑制糖尿病雄性大鼠的STAT3活化，改善肾小球滤过功能，可以防止糖尿病引起的组织病理学和超微结构改变。此外，尼呋沙嗪治疗可显着减少糖尿病肾组织中肾巨噬细胞的浸润和纤维化，并降低TNF-α和IL-18的mRNA和蛋白水平。目前的发现揭示了尼呋沙嗪作为一种主要通过STAT3抑制来阻碍糖尿病患者DN的发生和发展的替代抗炎疗法的功效。