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Dapsone Ameliorates Colitis through TLR4/NF-kB Pathway in TNBS Induced Colitis Model in Rat.

氨苯砜通过TLR4/NF-kB通路改善TNBS诱导的大鼠结肠炎模型的结肠炎。

  • 影响因子:2.10
  • DOI:10.1016/j.arcmed.2021.03.005
  • 作者列表:"Mohammad Jafari R","Shayesteh S","Ala M","Yousefi-Manesh H","Rashidian A","Hashemian SM","Sorouri M","Dehpour AR
  • 发表时间:2021-04-01
Abstract

BACKGROUND:Crohn's disease (CD), a type of inflammatory bowel disease (IBD), emerges with severe gastrointestinal (GI) tract inflammation, sometimes known as hostile abdomen. Conventional treatment of CD has several limitations such as insufficient response to treatment, and intolerable side effects of drugs. In addition, the high cost of biologic drugs prevents patients from continuing their treatment. Dapsone showed vigorous anti-inflammatory effects on the skin diseases, lung diseases and inflammatory diseases of the nervous system. Hence, we decided to investigate the effect of dapsone on animal model of CD. METHODS:In this study, colitis was induced by instillation of 2,4,6-trinitrobenzenesulfonic acid (TNBS) 100 mg/kg. Rats were treated with daily gavage of dapsone (10, 12.5 and 20 mg/kg). Seven days after induction of colitis, specimens were collected for pathological and molecular assessments. RESULTS:Dapsone (12.5 and 20 mg/kg) preserved the histologic architecture of the colon and prevented crypts irregularity. Additionally, it decreased tissue edema and hindered inflammatory cells infiltration. Besides, all doses of dapsone decreased tissue concentration of tumor necrosis factor α (TNF-α) and interferon γ (INFγ). Western blot revealed that dapsone could attenuate inflammation via downregulation of toll-like receptor 4 (TLR4) and dephosphorylation of nuclear factor kB (NF-kB). CONCLUSION:Based on these findings, dapsone attenuates inflammation and decreases TNF-α and INF-γ in animal model of CD. It acts through TLR4/NF-kB pathway to exert these effects.

摘要

背景: 克罗恩病 (CD) 是一种炎症性肠病 (IBD),伴有严重的胃肠道炎症,有时称为腹部不适。CD的常规治疗具有若干限制,例如对治疗的反应不足,以及药物的不可耐受的副作用。此外,生物药物的高成本使患者无法继续治疗。氨苯砜对皮肤疾病、肺部疾病和神经系统炎症性疾病具有强烈的抗炎作用。因此,我们决定研究氨苯砜对CD动物模型的影响。 方法: 在本研究中,通过滴注2,4,6-三硝基苯磺酸 (TNBS) 100 mg/kg诱导结肠炎。每天用氨苯砜 (10、12.5和20 mg/kg) 管饲处理大鼠。结肠炎诱导后7天,收集样本用于病理学和分子评估。 结果: 氨苯砜 (12.5和20 mg/kg) 保留了结肠的组织学结构,并防止了隐窝不规则。此外,它减少组织水肿和阻碍炎性细胞浸润。此外,所有剂量的氨苯砜降低肿瘤坏死因子 α (TNF-α) 和干扰素 γ (ifn γ) 的组织浓度。Western blot显示氨苯砜可通过下调toll样受体4 (TLR4) 和去磷酸化核因子kB (NF-kB) 减轻炎症反应。 结论: 氨苯砜能减轻CD动物模型的炎症反应,降低TNF-α 和INF-γ 水平。它通过TLR4/NF-kB途径发挥这些作用。

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影响因子:2.68
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DOI:10.1080/14656566.2020.1814255
作者列表:["Sawada H","Oeda T","Kohsaka M","Tomita S","Umemura A","Park K","Yamamoto K","Kiyohara K"]

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DOI:10.1007/s11033-021-06299-9
作者列表:["Louvrier A","Terranova L","Meyer C","Meyer F","Euvrard E","Kroemer M","Rolin G"]

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