The aim of present investigation was to elucidate the unrevealed beneficial role of diosgenin against an experimental model of TNBS (2,4,6-trinitrobenzenesufonic acid)-induced ulcerative colitis (UC). Colitis was induced in Sprague-Dawley rats by intrarectal administration of TNBS (in 50% ethanol). Then animals were treated with diosgenin (50, 100, and 200 mg/kg) for 14 days. Various biochemical, behavioral, molecular, and histological analysis was performed. Diosgenin significantly decreased (p < 0.05) TNBS-induced elevated colonic oxido-nitrosative damage, myeloperoxidase, hydroxyproline, mRNA expressions of proinflammatory cytokines (TNF-α, IL-1β, IL-6, and IFN-γ) and inflammatory markers (iNOs and COX-2) induced by TNBS. Western blot analysis relevated that TNBS-induced up-regulated protein expressions of NF-κB, IκBα, Bax, and Caspase-1 were markedly decreased (p < 0.05) by diosgenin treatment. It also markedly ameliorated the histological insults induced in the colon by TNBS. In conclusion, diosgenin exerts its colon-protective efficacy probably through the inhibition of NF-κB/IkB-α and Bax/Caspase-1 signaling pathways to experimental TNBS-induced ulcerative colitis.

Abbreviations

ANOVA: Analysis of variance; 5-ASA: 5-aminosalicylic acid; Bax: Bcl-2-associated X protein; COX-2: Cyclooxygenase-2; DAI: Disease Activity Index; DMSO: Dimethyl sulfoxide; GAPDH: Glyceraldehyde 3-phosphate dehydrogenase; GSH: Glutathione; HP: Hydroxyproline; IAEC: International Animal Ethics Committee; IBD: Inflammatory Bowel Disease; IBS: Inflammatory Bowel Syndrome; IL’s: Interleukin’s; IFN-γ: Interferon-gamma; IκBα: nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor-alpha; iNOs: Inducible nitric oxide synthase; LTB4: Leukotriene B4; MDA: Malondialdehyde; MPO: Myeloperoxidase; NO: Nitric Oxide; NF-κB: Nuclear Factor-κB; ROS: Reactive Oxygen Species; SOD: Superoxide Dismutase; TNBS: Trinitrobenzene Sulfonic Acid; TNF-α: Tumor necrosis factor-α

中文翻译：

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阐明薯os皂甙元在实验性TNBS诱导的结肠炎中的结肠保护功效：抑制NF-κB/IkB-α和Bax / Caspase-1信号通路。

本研究的目的是阐明薯os皂甙元对TNBS（2,4,6-三硝基苯磺酸）诱导的溃疡性结肠炎（UC）实验模型的有益作用。通过直肠内施用TNBS（在50％乙醇中）在Sprague-Dawley大鼠中诱发结肠炎。然后，用薯os皂苷元（50、100和200 mg / kg）处理动物14天。进行了各种生化，行为，分子和组织学分析。薯gen皂苷元显着降低（p < 0.05）TNBS诱导的结肠氧化亚硝化损伤升高，髓过氧化物酶，羟脯氨酸，促炎细胞因子（TNF-α，IL-1β，IL-6和IFN-γ）的mRNA表达以及炎症标志物（iNOs和COX-2）诱导由TNBS。Western blot分析表明，薯di皂苷元处理可使TNBS诱导的NF-κB，IκBα，Bax和Caspase-1蛋白表达上调（p <  0.05）。它也显着改善了TNBS在结肠中引起的组织学损伤。总之，薯os皂甙元可能通过抑制NF-κB/IkB-α和Bax / Caspase-1信号通路通向实验性TNBS诱导的溃疡性结肠炎发挥其结肠保护作用。

缩略语

方差分析：方差分析；5-ASA：5-氨基水杨酸；Bax：Bcl-2相关的X蛋白；COX-2：环氧合酶-2；DAI：疾病活动指数；DMSO：二甲基亚砜；GAPDH：3-磷酸甘油醛脱氢酶；GSH：谷胱甘肽；HP：羟脯氨酸；IAEC：国际动物伦理委员会；IBD：炎性肠病；IBS：炎症性肠综合症；IL：白介素；IFN-γ：γ-干扰素；IκBα：B细胞抑制剂α中κ光多肽基因增强子的核因子；iNOs：诱导型一氧化氮合酶；LTB4：白三烯B4；MDA：丙二醛；MPO：髓过氧化物酶；NO：一氧化氮；NF-κB：核因子-κB；ROS：活性氧；SOD：超氧化物歧化酶；TNBS：三硝基苯磺酸；TNF-α：肿瘤坏死因子-α