Ceftriaxone sodium was intragastrically administered for five days to establish an enteric dysbacteriosis model of mice. Mice were randomly divided into four groups: the model group, and the low-, medium-, and high-dose groups. The low-, medium-, and high-dose groups were intragastrically administered different doses of Bifidobacterium lactis V9 solution, whereas the normal control and model groups were administered the same volume of normal saline. Twenty-three days after administration, the composition and distribution of microorganisms in the feces of the mice were detected using viable count and 16S rRNA gene sequencing. An enzyme-linked immunosorbent assay kit was used to measure the levels of interleukin (IL)-1β, IL-6, tumor necrosis factor (TNF)-α, and IL-2 in serum and the levels of SOD, MDA, GSH, and GSH-Px in the small intestine and liver. HE staining was used to observe the histopathological changes in the small intestine. Thirty days after administration, the levels of IL-1β, IL-6, TNF-α, and IL-2 in the medium- and the high-dose groups were significantly lower than those in the model group (by 31.73, 17.04, 12.57 and 31.71 pg/mL, respectively); the MDA content in the small intestine and liver tissues in the high-dose group was significantly lower than that in the model group (p<0.01). The SOD, GSH, and GSH-Px levels in the middle- and high-dose groups significantly increased (p<0.01). B. lactis V9 significantly ameliorated the intestinal microflora imbalance caused by ceftriaxone sodium in mice. Fecal viable count indicated that the number of Enterobacter spp. significantly reduced (by 0.34 lg CFU/g) in the high-dose group. The numbers of Lactobacillus and Bifidobacterium spp. significantly increased (by 0.40 lg cfu/g and 0.26 lg cfu/g, respectively). The abundance of bacteria in the Alloprevotella and Weissella genera decreased significantly (p<0.01). Thus, B. lactis V9 effectively ameliorated the enteric dysbacteriosis caused by ceftriaxone sodium and regulated the diversity of intestinal microbiota.