低聚木糖对小鼠肠道菌群和短链脂肪酸的影响

EFFECTS OF XYLOOLIGOSACCHARIDES ON INTESTINAL FLORA AND SHORT-CHAIN FATTY ACIDS OF MICE

选取18~22 g BalB/C雄性小鼠,随机分为低、中、高剂量组和对照组共4组,剂量组连续14 d分别以0.12、0.23、0.70 g（/kg.BW）低聚木糖灌胃,对照组用等量无菌生理盐水灌胃.收集0、7、14 d小鼠粪便进行肠道菌群菌落数量及短链脂肪酸乙酸、丙酸、正丁酸和异丁酸含量的测定.结果表明,低聚木糖可以促进小鼠肠道益生菌双歧杆菌和乳酸杆菌的增殖,并抑制肠道中可能致病菌肠杆菌、肠球菌、产气荚膜梭菌的生长.在摄入0.23 g（/kg.BW）条件下,对双歧杆菌和乳酸杆菌的增殖作用最强,对肠球菌、产气荚膜梭菌的抑制生长作用最强;增加低聚木糖的摄入剂量,可以提高对肠杆菌生长的抑制.低聚木糖能够促进小鼠肠道代谢产生乙酸、丙酸和丁酸,提高肠道短链脂肪酸总量.灌胃14 d,乙酸含量在0.70 g（/kg.BW）剂量组中达到最高值131.2μmol/g;丙酸和丁酸含量在0.23 g（/kg.BW）剂量组中达到最高值1.57μmol/g和16.73μmol/g.

The tests were carried out by grouping 18 to 22 g BalB/C male mice into four groups randomly, intragastrically administrating 0 g/ （kg ·BW）, 0.12 g/ （kg ·BW）, 0.23 g/ （kg ·BW） and 0.70 g/ （kg ·BW） xylooligosaccharides to the testing groups continuously for 14 days, intragastrically administrating the same amount of sterile saline solution to the contrast group, collecting feces of the mice at 0, 7 and 14 days, and determining the number of intestinal flora colonies, and the contents of short-chain fatty acids （acetic acid, propionic acid, n-butyric acid and isobutyric acid）. The results showed that xylooligosaccharides could promote proliferation of Bifidobacterium and Lactobacillus, and suppress the reproduction of possible pathogenic Enterobacter, Enterococci and Clostridium perfringens. Xylooligosaccharides with the dose of 0.23 g/ （kg·BW） had the highest effects in promoting proliferation of Bifidobacterium and LactobociUus, and suppressing the reproduction of Enterococci and Clostridium perfringens. Xylooligosaccharides could promote intestinal metabolism to produce acetic acid, propionic acid and butyric acid so as to improve the contents of intestinal short-chain fatty acids. After intragastrically administration for 14 days, the acetic acid content reached the highest value （131.2 μmol/g） in the 0.70 g/ （kg·BW） dose group; and propionic acid and butyric acid contents respectively reached the highest values （1.57 μmol/g and 16.73 μmol/g） in the 0.23 g/（kg· BW） dose group.