Hubei Province Key Laboratory of Occupational Hazard Identification and Control, Institute of Pharmaceutical Innovation, School of Medicine, Wuhan University of Science and Technology, Wuhan 430065, China.
Mar Drugs. 2023 Jun 25;21(7):376. doi: 10.3390/md21070376.
The use of functional foods and their bioactive components is receiving increasing attention as a complementary and alternative therapy for chronic ulcerative colitis (UC). This study explored the protective effect and mechanisms of Eckol, a seaweed-derived bioactive phlorotannin, on the dextran sodium sulfate (DSS)-induced chronic UC in mice. Eckol (0.5-1.0 mg/kg) reduced DSS-enhanced disease activity indexes, and alleviated the shortening of colon length and colonic tissue damage in chronic UC mice. The contents of tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6 were significantly decreased, and the level of anti-inflammatory IL-10 was enhanced in the serum and colonic tissues collected from Eckol-treated mice compared with the DSS controls. Eckol administration significantly reduced the number of apoptotic cells and the expression of cleaved Caspase-3, and increased the B-cell lymphoma-2 (Bcl-2)/B-cell lymphoma-2- associated X (Bax) ratio in DSS-challenged colons. There were more cluster of differentiation (CD)11c dendritic cells and CD8 T cells, and less CD4 T cells infiltrated to inflamed colonic tissues in the Eckol-treated groups. Expression of colonic Toll-like receptor 4 (TLR4), nuclear factor kappa-B (NF-κB) p65, phosphorylated-signal transducer and activator of transcription (pSTAT)3 was significantly down-regulated by Eckol compared with the DSS-challenged group. In conclusion, our data suggest that Eckol appeared to be a potential functional food ingredient for protection against chronic UC. The anti-colitis mechanisms of Eckol might be attributed to the down-regulation of the TLR4/NF-κB/STAT3 pathway, inhibition of inflammation and apoptosis, as well as its immunoregulatory activity.
作为慢性溃疡性结肠炎(UC)的一种补充和替代疗法,功能性食品及其生物活性成分的应用越来越受到关注。本研究探讨了一种海藻来源的生物活性多酚——Eckol 对葡聚糖硫酸钠(DSS)诱导的慢性 UC 小鼠的保护作用及其机制。Eckol(0.5-1.0mg/kg)降低了 DSS 增强的疾病活动指数,并缓解了慢性 UC 小鼠结肠长度缩短和结肠组织损伤。与 DSS 对照组相比,Eckol 治疗组小鼠血清和结肠组织中肿瘤坏死因子(TNF)-α、白细胞介素(IL)-1β和 IL-6 的含量显著降低,抗炎性 IL-10 的水平升高。Eckol 给药显著减少了凋亡细胞的数量和Cleaved Caspase-3 的表达,并增加了 DSS 攻击结肠中的B 细胞淋巴瘤-2(Bcl-2)/B 细胞淋巴瘤-2 相关 X(Bax)的比值。在 Eckol 治疗组中,浸润到炎症性结肠组织中的 CD11c 树突状细胞和 CD8 T 细胞增多,而 CD4 T 细胞减少。与 DSS 攻击组相比,Eckol 显著下调了结肠 Toll 样受体 4(TLR4)、核因子 kappa-B(NF-κB)p65、磷酸化信号转导和转录激活因子(pSTAT)3 的表达。综上所述,我们的数据表明,Eckol 似乎是一种潜在的功能性食品成分,可用于预防慢性 UC。Eckol 的抗结肠炎机制可能归因于 TLR4/NF-κB/STAT3 通路的下调、炎症和细胞凋亡的抑制以及其免疫调节活性。