目的探究枸杞多糖（LBP）对溃疡性结肠炎（UC）的保护作用及其对肠道菌群的调节效应。方法将20只无特定病原 体（SPF）级及20只无菌（GF）级C57BL/6健康雄性小鼠各分成右旋葡聚糖硫酸钠（DSS）组（n=10，SPF）、LBP组（n=10，SPF）、GF（DSS） 组（n=10）和GF（LBP）组（n=10）。利用三循环间断饮用2% DSS 7 d，共54 d，建立UC模型。DSS组及GF（DSS）组小鼠全程正常饮 食，LBP组及GF（LBP）组全程给予1% LBP膳食补充。第54天，对各组小鼠进行UC表型评估（体重、结肠长度、疾病指数评分和 髓过氧化物酶活性），并采用应激排便法收集小鼠粪便，16S rRNA高通量测序分析肠道菌群组成，最后采用气相色谱‐质谱联用法 检测粪便中短链脂肪酸分子含量的变化。结果LBP显著增加了UC小鼠的体重和结肠长度，降低了疾病指数评分和髓过氧化物 酶活性，但是在GF级小鼠中LBP对UC的保护作用消失。16S rRNA测序结果显示，与DSS组相比，LBP组显著增加了益生菌乳杆 菌属（[ 0.55±0.38）×10‐2比（3.83±1.78）×10‐2，P=0.009]、未分类的毛螺菌属（[ 1.84±0.42）×10‐2比（3.90±1.36）×10‐2，P=0.023]、产丁酸球 菌属（[ 0.03±0.04）×10‐2比（0.11±0.01）×10‐2，P=0.007]以及未分类的S24‐7菌属（[ 9.91±1.44）×10‐2比（28.90±15.68）×10‐2，P=0.004]的 丰度。除此之外，LBP显著增加了UC小鼠粪便中丁酸的含量（[ 3.96±0.78）ng/mg比（7.44±1.67）ng/mg，P=0.022]。但是，LBP并未 增加GF级UC小鼠的丁酸含量（[ 6.02±0.13）ng/mg比（6.05±0.11）ng/mg，P=0.150]。结论LBP可以通过调节UC小鼠肠道菌群的组 成，促进菌群代谢物丁酸的产生而缓解肠道炎症。

Objective To investigate the protective effect of lycium barbarum polysaccharide (LBP) on ulcerative colitis and its regulatory effect on the intestinal flora. Method 20 specific⁃pathogen free (SPF) and 20 germ⁃free (GF) C57BL/6 healthy male mice were respectively divided into dextran sulphate sodium (DSS) group (n=10, SPF), LBP group (n=10, SPF), GF (DSS) group (n=10) and GF (LBP) group (n=10). The model of ulcerative colitis was established by discontinuously drinking 2% DSS for 7 days with three cycles, totally for 54 days. DSS and GF (DSS) groups were given a normal diet, while LBP and GF (LBP) groups were given 1% LBP dietary supplement throughout the whole process. Finally, the UC phenotype (body weight, colon length, disease index score and myeloperoxidase activity) were assessed in each group. And the feces of mice were collected by stress defecation method, and the composition of intestinal flora was analyzed by 16S rRNA high⁃throughput sequencing. The content of short⁃chain fatty acids in feces was detected by gas chromatography⁃mass spectrometry. Result LBP exerted a significant effect against UC, as indicated by increased body weight and colon length, and decreased disease activity index scores and myeloperoxidase activity. But the protective effect of LBP on UC was reversed in GF mice. The abundance of some probiotics, such as Lactobacillus [(0.55±0.38)×10⁃2 vs (3.83±1.78)×10⁃2, P=0.009], unclassified Lachnospiraceae [(1.84±0.42)×10⁃2 vs (3.90±1.36)×10⁃2, P=0.023], Butyricicoccus [(0.03±0.04)×10⁃2 vs (0.11±0.01)×10⁃2, P=0.007], unclassified S24⁃7 [(9.91±1.44) ×10⁃2 vs (28.90±15.68) ×10⁃2, P=0.004], increased obviously with LBP treatment. In addition, LBP significantly increased the content of butyric acid in the feces of mice with UC [(3.96±0.78) ng/mg vs (7.44±1.67) ng/mg, P=0.022]. However, LBP did not increase the content of butyric acid in GF mice [(6.02±0.13) ng/mg vs (6.05±0.11) ng/mg, P=0.150]. Conclusion LBP can alleviate DSS⁃induced UC by regulating the composition of intestinal flora and promoting the production of butyric acid.