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Therapeutic effect of the sulforaphane derivative JY4 on ulcerative colitis through the NF-kappa B-p65 pathway

机译:萝卜硫素衍生物JY4通过NF-κB-p65通路治疗溃疡性结肠炎的疗效

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摘要

The efficacy of the sulforaphane derivative JY4 was evaluated in acute and chronic mouse models of ulcerative colitis induced by dextran sodium sulfate. Oral administration of JY4 led to significant improvements in symptoms, with recovery of body weight and colorectal length, together with reduced diarrhoea, bloody stools, ulceration of colonic tissue and infiltration of inflammatory cells. The oral bioavailability of JY4, determined by comparing oral dosing with injection into the tail vein, was 5.67, which was comply with the idea in the intestinal function. Using a dual-luciferase reporter assay, immunofluorescence studies, western blot analysis and immunohistochemical staining, JY4 was shown to significant interfere with the NF-kappa B-p65 signaling pathway. By preventing the activation of NF-kappa B-p65, JY4 inhibited the overexpression of downstream inflammatory factors, thereby exerting an anti-inflammatory effect on the intestinal tract. This study thus provides a promising candidate drug, and a new concept for the treatment of ulcerative colitis. GRAPHICS .
机译:在葡聚糖硫酸钠诱导的溃疡性结肠炎急性和慢性小鼠模型中评估萝卜硫素衍生物JY4的疗效。口服JY4可显著改善症状,恢复体重和结直肠长度,同时减少腹泻,血便,结肠组织溃疡和炎症细胞浸润。通过比较口服剂量和尾静脉注射测定JY4的口服生物利用度为5.67%,符合肠道功能的思想。使用双荧光素酶报告基因测定、免疫荧光研究、蛋白质印迹分析和免疫组织化学染色,JY4 被证明显着干扰 NF-κ B-p65 信号通路。JY4通过阻止NF-κB-p65的活化,抑制下游炎症因子的过表达,从而对肠道产生抗炎作用。因此,本研究为溃疡性结肠炎的治疗提供了一种有前途的候选药物和新概念。[图形] .

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