Ulcerative colitis (UC) is the major type of inflammatory ailment with elevated prevalence worldwide. Dieckol (DEK) is a phlorotannin that is extensively found in marine algae and has been found to have different pharmacological properties. Nevertheless, the impact of DEK in UC has not been investigated earlier. Therefore, we appraised DEK's function in dextran sulfate sodium (DSS)-induced UC in the mouse. An overall of 30 mice was randomized into 5 equal groups. Control mice treated with a standard diet (group I), colitis mice challenged with 3% of DSS through drinking water for 7 consecutive days (group II), DEK was supplemented via oral gavage from day 1 to 10 at the dosages of 5, 10, and 15 mg/kg b.wt, respectively. All animals were sacrificed on the 11th day. The body weight (bwt), colon length, disease activity index, malondialdehyde (MDA), myeloperoxidase (MPO), and histological features were observed using suitable techniques, and COX-2 expression was investigated by immunohistochemistry. Moreover, TNF-α, IL-1β, p65, IκBα, HO-1, and Nrf2 expressions were measured using ELISA and RT-PCR techniques, respectively. DEK treatment to the colitis mice considerably lessened, DSS-challenged alterations in body weight, DAI, colonic length shortening and histological changes. DEK exhibited potent antioxidant effects due to the reduced MDA and MPO, and Nrf2 expression markers while the HO-1 marker was augmented. Additionally, DEK also suppressed the expression s of TNF-α, IL-1β, and the p-p65, p-IκBα, and p65 and augmented the expression of IκBα, which eventually proved the anti-inflammatory potential of DEK against the DSS-challenge. Based on these results, DEK has been found effective in mitigating colitis, conceivably alleviating colon inflammation through the NF-κB inhibition and triggering of Nrf2/HO-1 signaling cascade.

中文翻译：

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Dieckol 通过抑制炎症通路和激活 Nrf2/HO-1 信号通路减轻葡聚糖硫酸钠诱导的结肠炎

溃疡性结肠炎 (UC) 是主要类型的炎症性疾病，在世界范围内患病率升高。Dieckol (DEK) 是一种广泛存在于海藻中的根皮单宁，已被发现具有不同的药理特性。然而，DEK 在 UC 中的影响尚未得到更早的研究。因此，我们评估了 DEK 在葡聚糖硫酸钠 (DSS) 诱导的小鼠 UC 中的功能。总共 30 只小鼠被随机分成 5 个相等的组。用标准饮食处理的对照小鼠（I 组），结肠炎小鼠通过饮用水连续 7 天接受 3% DSS 攻击（II 组），从第 1 天到第 10 天通过口服灌胃补充 DEK，剂量为 5、10和 15 mg/kg b.wt，分别为。在第11天处死所有动物。体重（bwt）、结肠长度、疾病活动指数、使用合适的技术观察丙二醛 (MDA)、髓过氧化物酶 (MPO) 和组织学特征，并通过免疫组织化学研究 COX-2 表达。此外，分别使用ELISA和RT-PCR技术测量TNF-α、IL-1β、p65、IκBα、HO-1和Nrf2的表达。DEK 对结肠炎小鼠的治疗大大减轻了 DSS 挑战的体重、DAI、结肠长度缩短和组织学变化。由于减少了 MDA 和 MPO 以及 Nrf2 表达标记，而 HO-1 标记增加，DEK 表现出有效的抗氧化作用。此外，DEK 还抑制了 TNF-α、IL-1β 和 p-p65、p-IκBα 和 p65 的表达并增加了 IκBα 的表达，这最终证明了 DEK 对 DSS 的抗炎潜力。挑战。基于这些结果，