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Hecogenin and fluticasone combination attenuates TNBS-induced ulcerative colitis in rats via downregulation of pro-inflammatory mediators and oxidative stress
Immunopharmacology and Immunotoxicology ( IF 2.9 ) Pub Date : 2021-01-12
Deepa K. Ingawale, Satish K. Mandlik, Snehal S. Patel

Abstract

Objective

Ulcerative colitis is common types of severe, progressive, idiopathic inflammatory bowel disease that involves the mucosal lining of the large intestine. The purpose of the study is to explore the effects of hecogenin in TNBS (2, 4, 6- trinitrobenzene sulfonic acid) induced ulcerative colitis model in rats.

Material and methods

Thirty Wistar rats were randomized into five groups: (i) Normal Control (NC), (ii) Disease Control (DC), (iii) Hecogenin (HG) (50 µg/rat), (iv) Fluticasone (FC) (50 µg/rat), (v) Hecogenin + Fluticasone (HG + FC) combination (25 µg/rat). Colitis was induced by trans-rectal administration of TNBS using a catheter inserted 8 cm into the rectal portion of the rat. Colitis was evaluated by an independent observer who was blinded to the treatment. All treatment group results were compared to the TNBS group results.

Results

The study results revealed that treatment of rats with HG and HG + FC significantly improved the body weight and colon length whereas; decreased the spleen weight, colon weight/length ratio, macroscopic lesions score, diarrhea score and adhesion score. The drug treatment in rats substantially decreased the development of inflammatory cytokines, levels of serum immunoglobulin E, colonic nitric oxide contents and restoration of antioxidant stress markers. Histopathological colon sample study significantly reduced colonic inflammation with a substantial decrease in inflammation score.

Conclusion

Thus, HG and HG + FC combination could change the pathogenesis of the disease and may be a potential therapeutic target for the treatment of ulcerative colitis by a reduction in dose in conjunction with FC to prevent the persistent adverse effects associated with FC.



中文翻译:

血红素和氟替卡松的组合可通过下调促炎性介质和氧化应激来减轻TNBS诱导的大鼠溃疡性结肠炎

摘要

目的

溃疡性结肠炎是严重,进行性,特发性炎症性肠病的常见类型,涉及大肠的粘膜内层。这项研究的目的是探讨血红素在TNBS(2,4,6,三硝基苯磺酸)诱导的大鼠溃疡性结肠炎模型中的作用。

材料与方法

将30只Wistar大鼠随机分为五组:(i)正常对照(NC),(ii)疾病对照(DC),(iii)血红素(HG)(50 µg /大鼠),(iv)氟替卡松(FC)(50 (v)血红素+氟替卡松(HG + FC)组合(25微克/大鼠)。使用插入大鼠直肠部分8厘米的导管经TNBS经直肠给药可诱发结肠炎。结肠炎由对治疗不知情的独立观察员评估。将所有治疗组结果与TNBS组结果进行比较。

结果

研究结果显示,用HG和HG + FC治疗大鼠可显着改善体重和结肠长度,而 降低脾脏重量,结肠重量/长度比,宏观病变评分,腹泻评分和粘连评分。在大鼠中进行药物治疗后,炎症细胞因子的产生,血清免疫球蛋白E的水平,结肠中一氧化氮的含量以及抗氧化应激标志物的恢复都大大降低。组织病理学结肠样本研究显着减少了结肠炎症,同时炎症评分显着降低。

结论

因此,HG和HG + FC的组合可以改变疾病的发病机制,并且可以通过减少与FC结合的剂量来预防溃疡性结肠炎的持续副作用,从而成为治疗溃疡性结肠炎的潜在治疗靶标。

更新日期:2021-01-13
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