救必应抗炎活性评价及抗炎机制初探OA

Objective:To investigate the anti-inflammatory activity and mechanism of Jiubiying using zebrafish inflam-mation models and network pharmacology technology.Methods:Zebrafish inflammation models were established by copper sulfate immersion,tail amputation,and lipopolysaccharide microinjection.Neutrophil migration and aggregation were ob-served.Further evaluations of anti-inflammatory activity were performed using survival analysis,pathological morphology ob-servation,and quantitative real-time PCR.Finally,network pharmacology was used to predict the anti-inflammatory targets and signaling pathways of Jiubiying.Results:Jiubiying significantly inhibited neutrophil migration and aggregation toward inflammatory sites in zebrafish larvae induced by copper sulfate immersion,tail amputation,and lipopolysaccharide microin-jection.It improved the survival rate of lipopolysaccharide-inflamed zebrafish and reduced the expression of inflammatory cytokines interleukin-6(IL-6)and tumor necrosis factor-α(TNF-α).Network pharmacology analysis indicated that Jiubiy-ing exerted its anti-inflammatory effects mainly through components such as Jiubiying acid,ilexin A,crocetin dimethyl es-ter,and rotundifoline,acting on multiple core targets including tumor necrosis factor(TNF),signal transducer and activator of transcription 3(STAT3),matrix metalloproteinase 2(MMP2),epidermal growth factor receptor(EGFR),and serine/threonine kinase 1(NR3C1),primarily involving the relaxin signaling pathway,proteoglycans in cancer pathway,and focal adhesion pathway.Conclusion:Jiubiying exerts anti-inflammatory effects through a multi-component,multi-target,and multi-pathway mechanism,providing theoretical support for further research and development.