Atta Aamna, Naveed Muhammad, Rahman Mujeeb Ur, Alioui Yamina, Ansari Immad, Ali Sharafat, Ghaleb Eslam, Farooqui Nabeel Ahmed, Abusidu Mohammad, Xin Yi, Feng Bin
College of Basic Medical Science, Dalian Medical University, Dalian 116044, China.
Int J Mol Sci. 2025 Jul 16;26(14):6805. doi: 10.3390/ijms26146805.
Ulcerative colitis (UC) is a chronic inflammatory bowel disease driven by immune dysregulation, microbiota imbalance, and intestinal barrier dysfunction. Despite its global burden, effective therapies remain limited. This study explores the therapeutic potential of polysaccharides (ACP) in a dextran sulfate sodium (DSS)-induced murine colitis model. High-performance liquid chromatography (HPLC)-characterized ACP was administered orally to BALB/c mice following colitis induction. ACP treatment significantly reduced Disease Activity Index (DAI) scores, preserved colon length, and restored intestinal barrier integrity by upregulating tight junction proteins. Mechanistically, ACP modulated immune homeostasis, suppressing pro-inflammatory cytokines (IL-17, IL-23, CRP) while enhancing anti-inflammatory mediators (IL-4, TGF-β). Furthermore, ACP inhibited hepatic TLR4/MyD88/NF-κB signaling, attenuated systemic inflammation, and reshaped gut microbiota composition by enriching beneficial taxa and reducing pathogenic . These findings demonstrate ACP multi-target efficacy in colitis, positioning it as a promising natural therapeutic for UC.
溃疡性结肠炎(UC)是一种由免疫失调、微生物群失衡和肠道屏障功能障碍驱动的慢性炎症性肠病。尽管其全球负担沉重,但有效的治疗方法仍然有限。本研究在葡聚糖硫酸钠(DSS)诱导的小鼠结肠炎模型中探索了多糖(ACP)的治疗潜力。在诱导结肠炎后,将经高效液相色谱(HPLC)表征的ACP口服给予BALB/c小鼠。ACP治疗显著降低了疾病活动指数(DAI)评分,保留了结肠长度,并通过上调紧密连接蛋白恢复了肠道屏障完整性。从机制上讲,ACP调节免疫稳态,抑制促炎细胞因子(IL-17、IL-23、CRP),同时增强抗炎介质(IL-4、TGF-β)。此外,ACP抑制肝脏TLR4/MyD88/NF-κB信号传导,减轻全身炎症,并通过富集有益菌群和减少致病菌来重塑肠道微生物群组成。这些发现证明了ACP在结肠炎中的多靶点疗效,使其成为一种有前途的UC天然治疗药物。