金荞麦片对DSS诱导炎症模型小鼠炎症因子水平的影响

Effect of Fagopyrum Cymosum Tablets on the Level of Inflammatory Factor in DSS-induced Inflammation Model Mice

目的:观察金荞麦片对葡聚糖硫酸钠(dextran sulfate sodium,DSS)诱导的小鼠炎症性肠病的改善作用及机制。方法:20只SPF级C57BL/6小鼠随机分成对照组和金荞麦片组,两组小鼠给予自由饮用30 g·L-1 DSS连续7 d,同时每日给予对照组双蒸水、金荞麦片组金荞麦混悬液,均连续灌胃给药7 d。记录每日小鼠疾病活动指数,取材后测量结直肠长度及脾质量,HE染色后进行组织病理学评分,实时荧光定量PCR检测结直肠组织中肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)、白细胞介素-6(interleukin,IL-6)、IL-1β和IL-10相对表达量。结果:与对照组比较,金荞麦片组DAI评分在第5天和第6天显著降低(P<0.01);金荞麦片组结直肠长度显著长于对照组(P<0.05),且脾脏指数显著减小(P<0.01);金荞麦片组结直肠中TNF-α、IL-6和IL-1β水平显著低于对照组(P<0.05)。结论:金荞麦片可能通过下调促炎因子表达从而预防性的减轻DSS诱导的炎症模型小鼠的炎症性肠病的炎症症状及结直肠组织的炎性损伤。

Objective:To observe the effect and mechanism of fagopyrum cymosum tablets on inflammatory bowel disease induced by dextran sodium sulfate(DSS)in mice.Methods:20 SPF C57 BL/6 mice were randomly divided into control group and fagopyrum cymosum tablets group.The mice in the two groups were given free drinking of 30 g·L-1 DSS for 7 days,and double steamed water in the control group and golden buckwheat suspension in the fagopyrum cymosum tablets group were given daily for 7 days.Daily disease activity index of mice was recorded.Colon length and spleen quality were measured after sampling.Histopathological scores were scored after HE staining.Relative expressions of tumor necrosis factor-α(TNF-α),interleukin(IL-6),IL-1βand IL-10 in colorectal tissues were detected by real-time fluorescence quantitative PCR.Results:Compared with the control group,the DAI score of the fagopyrum cymosum tablets group decreased significantly on the 5 th and 6 th day(P<0.01);the colon and rectum length of fagopyrum cymosum tablets group was significantly longer than that of the control group(P<0.05),and the spleen index was significantly decreased(P<0.01);the levels of TNF-α,IL-6 and IL-1βin the fagopyrum cymosum tablets group were significantly lower than those of the control group(P<0.05).Conclusion:Fagopyrum cymosum tablets may prevent the inflammatory symptoms of DSS-induced inflammatory bowel disease and the inflammatory damage of colorectal tissue by down-regulating the expression of pro-inflammatory factors.