目的 探讨黄精（Rhizoma polygonati,RP）对葡聚糖硫酸钠（dextran sulfate sodium, DSS）诱导的溃疡性结肠炎（ulcerative colitis,UC）小鼠模型的保护作用及潜在机制。方法 将36只雄性C57BL/6小鼠随机分为6组：即对照组(CON)、模型组(DSS)、5-氨基水杨酸组[ 5-ASA,400 mg /（kg·d）]、RP低剂量组[ RP-L,2 g /（kg·d）]、RP中剂量组[ RP-M,4 g /（kg·d）]及RP高剂量 [ RP-H,8 g /（kg·d）],每组6只;除对照组正常饮水外,其余各组均自由饮用3.0 % DSS溶液进行UC造模,造模周期为7 d;从造模第3 d开始,5-ASA组及RP（L、M、H)组分别给予5-ASA或RP水煎液进行干预,持续7 d;实验期间,每天测量小鼠体重,并记录小鼠的粪便性状和便血情况,用于评估疾病活动指数 (disease activity index,DAI) 评分。实验结束后处死小鼠,测量结肠长度,酶联免疫吸附试验 (ELISA) 检测结肠组织中肿瘤坏死因子-α（tumor necrosis factor-α,TNF-α）、白细胞介素（interleukin,IL）-6、白细胞介素-1β、IL-10及髓过氧化物酶（myeloperoxidase,MPO）的水平,HE染色评估结肠组织损伤情况。结果 与CON组相比,RP-H干预降低了DAI评分（P <0.05）,缓解了结肠缩短（P <0.05）,同时下调IL-6、IL-1β、TNF-α 的表达,上调IL-10的表达（P <0.05）,抑制了MPO 的活力;HE染色病理结果显示,RP-H干预能减轻结肠组织炎症细胞浸润,促进杯状细胞修复。结论 RP可以有效调节炎症因子表达,减少结肠组织的炎症损伤,其机制可能与抑制炎症反应有关。
Abstract
Objective To investigate the protective effects of Rhizoma polygonati (RP) on dextran sulphate sodium (DSS)-induced ulcerative colitis (UC)and the underlying mechanisms. Methods Thirty-six male C57BL/6 mice were randomly divides into six groups (n=6 per group): control group (CON), model group (DSS), 5-aminosalicylic acid group(5-ASA, 400 mg/(kg·d)), low-dose RP group (RP-L, 2 g/(kg·d)), medium-dose RP group (RP-M, 4 g/(kg·d)], and high-dose RP group (RP-H, 8 g/(kg·d)]. Except for the CON, which received normal drinking water, all other groups were given 3.0 % DSS solution ad libitum for 7 days to induce UC. Starting from day 3 of modeling, the 5-ASA and RP groups were administed with 5-ASA or RP for 7 consecutive days. Body weight was recorded daily, and stool consistency and fecal bleeding were assessed to calculate the disease activity index (DAI) score. At the end of the experiment, mice were euthanized, and colon length was measured. Levels of tumor necrosis factor-α (TNF-α), interleukin (IL) -6, IL-1β, IL-10, and myeloperoxidase (MPO) in colon tissue were determined by enzyme-linked immunosorbent assay (ELISA). Colon tissue injury was evaluated by hematoxylin and eosin (HE) staining. Results Compared with the CON group, RP-H treatment significantly reduced the DAI score (P<0.05), alleviated colon shortening (P<0.05), downregulated the expression of IL-6, IL-1β, and TNF-α, upregulated IL-10 expression (P<0.05), and suppressed MPO activity. Histopathological examination revealed that RP-H intervention attenuated inflammatory cell infiltration and promoted goblet cell regeneration in colon tissue. Conclusion RP can effectively reduce colonic tissue injury in DSS-induced UC mice, party through the suppression of inflammatory responses.
关键词
黄精 /
溃疡性结肠炎 /
膳食干预 /
炎症因子 /
功能性食品
Key words
Rhizoma polygonati /
ulcerative colitis /
inflammatory factors
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