中图分类号 R285.5；R965 文献标志码A 文章编号 1001-0408(2025)14-1709-08

    DOI 10.6039/j.issn.1001-0408.2025.14.04

    ABSTRACTOBJECTIVETo explore thepotential mechanisms of astragalin(AG)in allvatingulcerativecolitis(UC)in mice throughmodulationof the intestinalflora.METHODSMale C57BL/6 micewererandomly divided intonormal group(CON group)，model group[dextran sodium sulfate(DSS)group]，5-aminosalicylic acid group(5-ASA group)，AG low-dose groupand high-dosegroup(AGLandAGH groups)，with8micein each group.Themice UCmodel was establishedby drinking 3% DSS solution continuously for 7 days in all groups except the CON group. After that， 3% DSS solution was replaced by water，and the mice of eachdrug group were gavaged with the corresponding drug solution. Micein the CONand DSS groups were gavaged with anequalvolumeofnormal saline，onceaday，for7days.Afer thelastgavage，thebodyweightchange index，diseaseactivity index(DAI) score，colon length and spleen index，and levels of inflammatory factors(tumor necrosis factor- ∝ ，interleukin- ?1β ， interleukin-6)werecomparedamongthemiceineachgroup；pathologicalchangesincolonictissesof themicewereobservedin eachgroup ......