抗性糊精(resistant dextrin,RD)可调节肠道健康,对溃疡性结肠炎(ulcerative colitis, UC)影响较大。该研究探讨了RD对葡聚糖硫酸钠(dextran sulfate sodium,DSS)诱导的急性UC小鼠的保护作用。雄性7周龄C57BL/6 J小鼠随机分为3组,分别为对照组(饮无菌水,10 mL/kg生理盐水灌胃)、模型组(饮3% DSS水,10 mL/kg生理盐水灌胃)和抗性糊精组(饮3% DSS水,3.25 g/kg RD灌胃),持续7 d,记录小鼠体重、疾病活动指数(disease activity index,DAI)评分;检测小鼠结肠组织病理、血清炎症因子、结肠黏蛋白2(mucin 2, MUC2)、紧密连接蛋白表达和肠道菌群改变。与模型组相比,抗性糊精可显著逆转UC小鼠体重降低、DAI评分升高、结肠缩短、脾脏肿大、血清炎症因子浓度升高和结肠组织炎性浸润(P<0.05),可部分恢复肠道屏障完整性;抗性糊精可降低急性UC小鼠肠道Turicibacter、Oscillospira和Akkermansia菌属的丰度,升高Lactobacillus的丰度。抗性糊精可改善急性结肠炎小鼠的症状,降低血清促炎因子水平和保护肠道黏膜屏障,其潜在的机制可能与调节肠道微生物,促进肠道有益菌繁殖、抑制条件致病菌和有害菌过度生长有关。
Resistant dextrin (RD) could regulate gut health, while less research on its effects on ulcerative colitis (UC). This study aimed to investigate the protective effects of RD on dextran sulfate sodium (DSS)-induced acute UC mice. Male 7-week-old C57BL/6J mice were randomly divided into three groups, including the control group (drinking sterile water, 10 mL/kg normal saline oral gavage), the DSS group (drinking 3% DSS, 10 mL/kg normal saline oral gavage) and DSS-RD group (drinking 3% DSS, 3.25 g/kg RD oral gavage) for seven days, and recorded the body weight and disease activity index (DAI) score, detected the pathological damage of the colon tissue, serum inflammatory cytokines, colonic mucin2 (MUC2) and tight junction protein expression, and gut microbiota changes. Results showed that compared with the DSS group, resistant dextrin could significantly reverse the weight loss, DAI scores elevation, colon shortening, spleen enlargement, serum pro-inflammatory cytokines concentration elevation, and colonic tissue inflammatory infiltration in colitis mice (P<0.05), and could partially restore the intestinal barrier integrity. Resistant dextrin decreased the abundance of Turicibacter, Oscillospira, and Akkermansia in acute colitis mice, and increased the abundance of Lactobacillus. Resistant dextrin could improve the symptoms of acute colitis mice, reduce the level of serum pro-inflammatory cytokines, and protect the intestinal mucosal barrier. The underlying mechanism may be related to regulating intestinal microbes, promoting the proliferation of probiotics and inhibiting the overgrowth of conditioned pathogens and harmful bacteria.
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