中文摘要：

目的：观察党参多糖对5-氟尿嘧啶（5-FU）引起的肠道炎症的治疗作用及探讨其作用机制。方法：将小鼠随机分为正常组、对照组、高、中、低剂量党参多糖组。对照组和多糖组用5-FU造模,多糖组给予口服党参多糖干预。观测小鼠每天的大便和体重情况;将小鼠处死后,取小鼠空肠,切片后测量其绒毛高度、隐窝深度、计算其绒毛高度/隐窝深度比值,测定小肠组织白细胞介素-1β（IL-1β）、白细胞介素-6（IL-6）、肿瘤坏死因子-α（TNF-α）的含量水平。结果：3组多糖组第4天相比对照组体重百分比下降受抑制,且有显著差异（P〈0.05或P〈0.01）。高、中剂量组第4天相比对照组大便得分具有显著差异（P〈0.05）。与对照组相比,多糖组显著抑制5-FU引起的小肠肠绒毛缩短、隐窝深度加深、绒毛高度/隐窝深度比值减少（P〈0.01）。多糖组TNF-（IL-1β、IL-6水平显著低于对照组（P〈0.01）。结论：党参多糖对5-FU引起的肠道黏膜炎有显著的治疗作用,其作用机制可能是通过抑制TNF-（IL-1β、IL-6等炎症因子的水平产生抗炎作用有关。

英文摘要：

Objective： To observe the therapeutic effect of radix codonopsi polysaccharide（ RCP） on 5- Fluorouracil（ 5- FU）- induced gastrointestinal mucositis and explore the underlying mechanism. Methods： The mice were randomly divided into normal control（ NC） group,positive control（ PC） group,low- dose polysaccharide（ LP） group,middle- dose polysaccharide（ MP） group and high- dose polysaccharide（ HP） group. The mice of NC and three polysaccharide groups were intragastrically administered 5- Fu on day 0 and the three polysaccharide groups were combined with CCP at the dose of 100 mg/kg,50 mg/kg and 25 mg/kg once a day for 5 days,respectively. Body weight and scoring for diarrhea index were recorded. After treatment for 4 days,TNF- α,IL- 6 and IL- 1β levels in the intestinal tissue were determined by ELISA. Results： On 4th day compared with PC group,body weight loss in MP group and HP group was inhabited significantly（ P〈0. 05 or P〈0. 01） and diarrhea scores in NC group as well as 3 model groups were decreased（ P〈0. 05）. Moreover,the treatment with RCP significantly inhibited the shortening effect of villus heights,crypts depths of small intestine and the ratio of villus heights to crypts depths induced by 5- Fu（ P〈0. 01）. The levels of TNF-（,IL- 1β,IL6 in 3 dose polysaccharide group were significantly decreased in comparison with PC group（ P〈0. 05 or P〈0. 01）. Conclusion： Our results suggest that RCP shows certain therapeutic effect on intestinal mucositis associated with chemotherapy by inhibiting intestinal the inflammation and down- regulating levels of TNF- α,IL- 6 and IL- 1β.