来自Costaria costata的Fucoidan通过抑制树突细胞激活来缓解硫酸诱导的性结肠炎
Wei Zhang1, Eun-Koung An2, So-Jung Kim2
1Shanghai Public Health Clinical Center, Shanghai Medical College, Fudan University, Shanghai, 201508, China.
International journal of biological macromolecules
|January 15, 2026
概括
来自Costaria costata (FCC) 的富科伊丹通过减少结肠炎症,有效治疗性结肠炎 (UC). 它通过向树突细胞和T细胞活动来起作用,显示为炎症性肠道疾病的自然疗法.
科学领域:
- 海洋生物技术 海洋生物技术
- 免疫学 免疫学 免疫学
- 胃肠病学 胃肠病学
背景情况:
- 富科伊丹是一种海藻多糖,表现出各种生物活动.
- 众所周知,来自Costaria costata (FCC) 的富科伊丹可以抑制树突细胞 (DC) 激活,并减少肺炎.
- 性结肠炎 (UC) 是一种慢性炎症性肠病,影响结肠.
研究的目的:
- 在UC的小鼠模型中研究口服FCC的抗炎作用.
- 阐明FCC在UC的背景下调节免疫反应的机制.
主要方法:
- 在小鼠中使用硫酸 (DSS) 诱导UC.
- 用FCC口服给DSS治疗的小鼠.
- 对结肠组织进行免疫细胞透 (T细胞,中性粒细胞) 的分析.
- 在结肠T细胞中测量细胞因子 (IFN-γ,IL-17) 的产生.
- 在中腔淋巴结 (mLN) DCs中评估DC激活标记物 (协同刺激剂,MHC分子).
- 在体外评估FCC对LPS诱导的DC激活和随后的T细胞反应的影响.
主要成果:
- 口服FCC剂量显著降低了DSS治疗小鼠的UC严重程度.
- FCC降低了T细胞和中性粒细胞进入结肠的透率.
- 美国FCC抑制了肠道T细胞中DSS诱导的干扰素 (IFN-γ) 和介质蛋白17 (IL-17) 的产生.
- FCC减少了mLN中的DC数量,并抑制了它们的激活 (共刺激剂和MHC分子的上调).
- FCC抑制了LPS诱导的DC激活,导致T细胞增殖和分化减少.
结论:
- 口服FCC通过调节DC和T细胞活性来缓解实验性性结肠炎.
- FCC显示出作为治疗肠道炎症的治疗剂的潜力,特别是UC.
- 向直流激活是FCC在肠道中抗炎作用的关键机制.
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