Lu Yanfei, Wu Rihui, Liu Jiaquan, Huang Jinwen, Liu Qiu, Yao Min, Wu Jingyu, Ye Jiming, Li Dongli, Gan Lishe, Jin Jingwei
School of Pharmacy and Food Engineering, Guangdong Provincial Key Laboratory of Large Animal Models for Biomedicine, Wuyi University, Jiangmen, PR China.
International Healthcare Innovation Institute (Jiangmen), Jiangmen, PR China.
Nat Prod Res. 2024 Dec 1:1-7. doi: 10.1080/14786419.2024.2435535.
This study investigated the therapeutic mechanism of Millettia Speciosa Champ. polysaccharide (MSCP), also known as Niu Dali polysaccharide, in treating ulcerative colitis (UC) using a dextran sulphate sodium (DSS) induced colitis model in C57BL/6 mice. Mice were randomly assigned to four groups: control, DSS model, and low- and high-dose MSCP treatment groups (50, 100 mg/kg/day, respectively). MSCP administration began concurrently with DSS induction. Throughout the intervention, changes in body weight and disease activity index were monitored. On day 44, colonic tissues were collected for analysis after measuring their lengths. Results demonstrated that MSCP effectively ameliorated DSS-induced chronic colitis by suppressing proinflammatory cytokine secretion, enhancing anti-inflammatory cytokine production, restoring intestinal epithelial barrier integrity, and downregulating TLR4 expression.
本研究利用葡聚糖硫酸钠（DSS）诱导的C57BL/6小鼠结肠炎模型，探究了美丽鸡血藤多糖（MSCP，又称牛大力多糖）治疗溃疡性结肠炎（UC）的作用机制。将小鼠随机分为四组：对照组、DSS模型组以及低剂量和高剂量MSCP治疗组（分别为50、100mg/kg/天）。MSCP给药与DSS诱导同时开始。在整个干预过程中，监测体重和疾病活动指数的变化。在第44天，测量结肠组织长度后收集组织进行分析。结果表明，MSCP通过抑制促炎细胞因子分泌、增强抗炎细胞因子产生、恢复肠道上皮屏障完整性以及下调TLR4表达，有效改善了DSS诱导的慢性结肠炎。
