The anti-inflammatory activity of eckol, a phlorotannin constituent of marine brown algae, has been widely demonstrated. Here, we found eckol at doses of 0.5–1.0 mg/kg protected against development of dextran sulfate sodium (DSS)-induced acute experimental colitis in mice. DSS-elevated colonic tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6 levels as well as nuclear factor kappa B(NF-κB)p65 and Toll like receptor (TLR)-4 expression were significantly suppressed, the colonic IL-10 level was enhanced in the eckol-treated mice. TUNEL-positive cells and Caspase-9 expression were downregulated in eckol-treated colons compared to DSS controls. Eckol inhibited the growth of potential gut pathogens and increased beneficial bacteria in colitic mice, and recruited CD11c⁺ dendritic cells (DCs) into inflamed colonic tissues. Colonic expression of regenerating islet-derived 3 gamma (Reg3g) was significantly increased by eckol. Overall, eckol represents a treatment alternative in colitis management. The induction of colonic Reg3g may account for the anti-inflammatory, anti-apoptotic, antimicrobial and immunoregulatory activities of eckol in colitic mice.

eckol是海洋褐藻中的phrotrotannin成分，具有抗炎活性。在这里，我们发现浓度为0.5–1.0 mg / kg的eckol可以防止硫酸葡聚糖硫酸钠（DSS）诱导的小鼠急性实验性结肠炎的发展。DSS升高的结肠肿瘤坏死因子（TNF）-α，白介素（IL）-1β，IL-6水平以及核因子κB（NF-κB）p65和Toll样受体（TLR）-4表达被显着抑制，经eckol处理的小鼠结肠IL-10水平升高。与DSS对照相比，在接受eckol处理的结肠中TUNEL阳性细胞和Caspase-9表达下调。Eckol抑制了肠道细菌中潜在的肠道病原体的生长并增加了有益细菌，并募集了CD11c ⁺树突状细胞（DC）进入发炎的结肠组织。eckol可显着提高再生胰岛来源的3 gamma（Reg3g）的结肠表达。总体而言，eckol代表结肠炎管理中的另一种治疗方法。结肠Reg3g的诱导可能解释了eckol在结肠小鼠中的抗炎，抗凋亡，抗微生物和免疫调节活性。