该研究探讨了鱼腥草多酚对溃疡性结肠炎小鼠的改善效果。50只KM雄性小鼠随机分为空白组、模型组、鱼腥草多酚低、中、高剂量组。使用浓度为3.5%的葡聚糖硫酸钠（dextran sulphate sodium，DSS）溶液连续灌胃9 d制备小鼠肠炎模型。造模后第3 d灌胃给药，每天1次，连续10 d。观察小鼠体重变化、结肠组织形态学改变和疾病活动指数（disease active index，DAI)；采用酶联法（ELISA）测定血清中炎症因子：肿瘤坏死因子（TNF-α），白细胞介素1β（IL-1β），白细胞介素（IL-6），γ干扰素（IFN-γ）；试剂盒检测小鼠血清中肝肾生化指标：血清丙氨酸转氨酶（ALT）、天冬氨酸转氨酶（AST）、血尿素氮（BUN)、血肌酐（Cr）。分析发现，与模型组相比，鱼腥草多酚干预组小鼠的便血减轻、结肠平均增加至8.35 cm（低剂量组）、9.53 cm（中剂量组）、10.87 cm（高剂量组）。DAI指数分别降低了29.83%、46.45%、54.82%。血清中TNF-α、IL-1β、IL-6、IFN-γ表达水平显著降低（p<0.01）。同时，鱼腥草多酚各剂量组降低了ALT、AST、Cr、BUN水平（p<0.05）。鱼腥草多酚可以有效改善DSS诱导KM雄性小鼠溃疡性结肠炎，降低血清促炎因子水平，其机制可能与抑制NF-κB相关。

In the current study, the ameliorating effect of total polyphenol from Houttuynia cordataon mice with ulcerative colitis was studied. 50 male KM mice were randomly divided into control group, modelgroup, low-, medium- and high-dose groups of polyphenol in Houttuynia cordata. The model group was induced by administering 3.5% dextran sodium sulphate (DSS) for 9 days. On third day, the polyphenol groups were infused to stomach after DSS administration for another 10 days. The changes of mice body weight, colonic histomorphology and the disease activity index (DAI) of each group were observed. The levels of TNF-α, IL-1β, IL-6, IFN-γ in serum were detected by ELISA. The expressions of aspartate aminotransferase (AST), aspartate transaminase (ALT), creatinine (Cr) and blood urea nitrogen (BUN) in serum were measured. Compared with the DSS group, polyphenol groups significantly reduced symptoms with bloody stool. Disease activity index (DAI) decreased to 29.83%, 46.45% and 54.82%, respectively. The mice colon increased to 8.35 cm (in low dose group), 9.53 cm (in medium dose group), and 10.87 cm (in high dose group) on average. Also, treatment with polyphenol considerably the ALT and AST level and the expression of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6) were decreased. These results demonstrate that polyphenol in Houttuynia cordata has an ameliorative effect on colonic damage, and decrease the level of serum proinflammatory factor. The mechanism may be related to inhibiting the activation of NF-κB.

山东省自然科学基金项目（ZR2020MC126）；山东省抗体制药协同创新中心开放课题（CIC-AD1816）；山东省教育厅研究生教学改革重点项目（SDYJG19056）