长短链菊粉对抗生素诱导肠道菌群紊乱小鼠调节作用的研究

Regulatory effects of long-and short-chain inulins on antibiotic-induced intestinal dysbiosis in mice

目的采用头孢曲松钠诱发小鼠肠道菌群紊乱建立模型,观察不同剂量长短链菊粉对抗生素诱导的肠道菌群紊乱小鼠的调节作用。方法 2g/(kg·d)头孢曲松钠灌胃小鼠,连续8d,诱导小鼠肠道菌群紊乱,然后将菌群紊乱小鼠分为低剂量短链菊粉处理组、高剂量短链菊粉处理组、低剂量长链菊粉处理组、高剂量长链菊粉处理组和自然恢复组,连续处理2周,采用PCR-DGGE和菌落计数的方法观察各组小鼠肠道菌群的恢复情况。结果抗生素处理后,小鼠肠道菌群与正常小鼠相比具有显著差异,菌群条带数明显减少(P<0.05),有益菌肠杆菌、乳酸杆菌、双歧杆菌和消化球菌含量明显减少(P<0.05),条件致病菌葡萄球菌和铜绿假单胞菌含量明显增多(P<0.05);经菊粉处理后,小鼠的肠道菌群恢复效果明显好于自然恢复组(P<0.05),其中长链菊粉处理组优于短链菊粉处理组,且高剂量长链菌粉处理组恢复程度优于低剂量长链处理组。结论菊粉能够有效调节抗生素引起的肠道菌群紊乱,而长链菊粉的调节作用优于短链菊粉,且高剂量更有效。

Objective To evaluate the regulatory effect of different doses of long-and short-chain inulins on mice intestinal dysbiosis induced by ceftriaxone sodium.Methods Ceftriaxone[2g/（kg·d）]was given to the mice intragastrically for 8days to build the model of intestinal dysbacteriosis.Then the mice were divided into 5groups respectively：low-dose long-chain inulin group,high-dose long-chain inulin group,low-dose short-chain inulin group,high-dose short-chain inulin group and spontaneous recovery group.The PCRDGGE and colony counting methods were used to observe the recovery of intestinal flora in each group.Results After treated with high dose of ceftriaxone,the intestinal flora of mice was significantly different from that of healthy mice,indicating by obviously decreased amount of intestinal beneficial bacteria such as Lactobacillus,Bifidobacteriumand Peptococcus（P〈0.05）and increased amount of conditional pathogens such as Staphylococcus and Pseudomonas aeruginosa（P〈0.05）.After treated with inulin,the intestinal flora of the mice was significantly recovered compared to the spontaneous receovery group,with the longchain inulin group better than the short-chain inulin group,and the high-dose long-chain group superior to low-dose long-chain group.Conclusion Inulin can effectively regulate intestinal flora disturbance caused by antibiotics,and the regulatory effect of long-chain inulin is better than that of short-chain inulin,with high dose beingmore effective.