Ulcerative colitis (UC) is a disease of increased worldwide prevalence. UC progression is associated with serious complications that leave the patient with considerable health burdens. Nifuroxazide is an oral nitrofuran antibiotic used as antidiarrheal medication. The current study places an emphasis on investigating the potential therapeutic effectiveness of nifuroxazide (10 mg/kg) and (20 mg/kg) against acetic acid (AA)-induced UC. Intra-rectal AA induced a significant colonic injury and impairment of colonic biochemical and functional incidences. Nifuroxazide in a dose-dependent manner significantly corrected UC associated injury. Macroscopic scoring of UC, serum lactate dehydrogenase (LDH) activity, C-reactive protein (CRP) titer, colon malondialdehyde (MDA) and total nitric oxide (NOx) contents significantly declined. Meanwhile, serum total antioxidant capacity (TAC) and colon catalase, superoxide dismutase (SOD) and glutathione transferase (GST) activities and reduced glutathione (GSH) concentration significantly increased in a dose-dependent way. Ultimately, histopathological, immunohistochemical and ultramicroscopic analysis of colon specimen revealed significant improvement. To pinpoint the mechanistic pathway underlying the curative effect of nifuroxazide, colon expression of NF-κB, caspase-3 was evaluated along with STAT-3 activation. Nifuroxazide induced a dose-dependent significant suppression of NF-κB and caspase-3 signaling together with STAT3 signaling. In conclusion; nifuroxazide can be proposed as a therapeutic candidate to attenuate UC and its associated symptoms. The potential underlying mechanism involves suppression of NF-κB/STAT-3/caspase- signaling.

溃疡性结肠炎（UC）是一种全球性流行病。UC进展与严重并发症相关，使患者承受相当大的健康负担。尼呋拉嗪是一种口服硝基呋喃抗生素，用作止泻药。当前的研究重点是研究尼古拉嗪（10 mg / kg）和（20 mg / kg）对乙酸（AA）诱导的UC的潜在治疗效果。直肠内AA引起明显的结肠损伤，并损害结肠生化和功能发生率。尼呋拉嗪以剂量依赖性方式显着纠正了UC相关损伤。UC的宏观评分，血清乳酸脱氢酶（LDH）活性，C反应蛋白（CRP）滴度，结肠丙二醛（MDA）和一氧化氮（NOx）含量显着下降。与此同时，血清总抗氧化剂能力（TAC）和结肠过氧化氢酶，超氧化物歧化酶（SOD）和谷胱甘肽转移酶（GST）活性以及降低的谷胱甘肽（GSH）浓度均呈剂量依赖性增加。最终，结肠标本的组织病理学，免疫组化和超显微分析显示出明显的改善。为了查明尼呋拉嗪治疗效果的机制途径，评估了NF-κB，caspase-3的结肠表达以及STAT-3的激活。尼呋沙嗪可诱导剂量依赖性的NF-κB和caspase-3信号转导以及STAT3信号转导抑制。结论; 尼呋拉嗪可被提议作为减轻UC及其相关症状的治疗候选药物。潜在的潜在机制涉及抑制NF-κB/ STAT-3 / caspase信号传导。