Background　and　aims:　Studies　have　shown　that　improving　the　intestinal　flora　can　alleviate　the　progression　of　liver　fibrosis.　Cordycepin　has　shown　potential　anti-inflammatory　and　anti-fibrosis　effects.　In　this　study,　we　aimed　to　investigate　the　effects　of　cordycepin　on　liver　fibrosis　and　how　it　affects　the　intestinal　flora　composition　to　determine　a　potentially　effective　therapeutic　approach　for　liver　fibrosis.　Experimental　procedure:　C57BL/6　mice　were　fed　a　special　diet　containing　3,5-diethoxycarbonyl-1,4-dihydroxylidine　(DDC)　to　induce　liver　fibrosis.　The　histopathological　changes　in　liver　tissue　and　intestinal　mucosa　were　determining　via　immunohistochemical　staining.　Serum　transaminase　levels　were　determined　using　biochemical　test　kits.　Faecalibaculum　samples　were　sequenced　via　16S　rRNA　sequencing.　Results:　Cordycepin　reduced　DDC-induced　liver　collagen　deposition,　improved　serum　alanine　aminotransferase　(ALT)　and　aspartate　aminotransferase　(AST)　levels,　and　reduced　the　levels　of　endothelial　dysfunction　markers　vascular　cell　adhesion　molecule　1　(VCAM)　and　thrombomodulin　(TM).　Our　analysis　of　the　intestinal　flora　composition　showed　that　Dubosiella,　Faecalibaculum,　and　Bifidobacterium　were　significantly　increased　in　the　cordycepin-treated　group　(P　＜　0.05).　The　Dubosiella　level　was　significantly　negatively　correlated　with　TM　and　VCAM　levels,　and　serum　levels　of　ALT　and　AST　(P　＜　0.05).　After　treatment　with　cordycepin,　the　microvilli　length　in　the　intestinal　mucosa,　the　density　of　goblet　cells,　and　the　expressions　of　occludin　and　zonula　occludens　protein　1　(ZO-1)　were　significantly　increased　(P　＜　0.05).　Conclusion:　We　discovered　that　cordycepin　improves　liver　fibrosis　in　vivo.　We　found　that　Dubosiella　levels　were　considerably　increased　in　the　cordycepin-treated　group　and　were　significantly　negatively　correlated　with　liver　sinusoidal　endothelial　damage.