To investigate the molecular mechanism of emodin in the treatment of sepsis-associated acute kidney injury (SA-AKI) by data mining and animal experiments.Critical genes in the pathogenesis of SA-AKI were screened from the GEO database for GO and KEGG enrichment analysis,and then PPI networks were constructed using STRING,and core target,inflammatory signaling pathway interaction networks were constructed using MCODE in Cytoscape.Wistar rats were used to construct three groups of models:sham operation group (Sham),sepsis group (CLP) and drug group (CLP + EMO).HE staining,urease,sarcosine oxidase,thiobarbituric acid,ELISA and Western blot were used to detect the three groups of models.The results showed that a total of 2 801 key targets for the pathogenesis of SA-AKI were obtained.GO biological process analysis suggests that the biological functions of these targets mainly involve membrane signal transduction,vascular regulation,and wound healing.KEGG pathway enrichment analysis showed that TNF,IL-17,PI3K - Akt,NF-κB and MAPK signaling pathways were enriched signaling pathways associated with inflammation.There was no difference in mortality within 6 days among the three groups (P>0.05).Compared with the sham group,glomeruli in the CLP group varied in size,with atrophy and division,tubular dilatation,vacuole-like changes were more common,and inflammatory cell infiltration was observed at high magnification;Scr,BUN,and MDA levels in the blood were significantly increased (P<0.001);cytokines TNF-α,IL-17,and IFN-γ levels were significantly increased (P<0.001);and TNF-α,IL-17A,TRAF6,and NF-κB signaling pathway protein expression was up-regulated in the renal tissue (P<0.05).Compared with the CLP group,vacuolated changes were decreased and inflammatory cell infiltration was decreased in the CLP + EMO group at high magnification;the above indexes measured in blood and the protein content expression measured in renal tissue showed different degrees of decrease (P<0.01,P<0.001 and P<0.05).In summary,emodin can improve renal function levels and reduce the inflammatory response in SA-AKI,which may be related to the down-regulation of IL-17/NF-κB signaling pathway and TNF/NF-κB signaling pathway.