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BackgroundKaempferol is a common avonoid aglycone widely found in plants. It exhibits bene cial therapeutic effects in the treatment of arthritis. However, the effects of kaempferol on gouty arthritis (GA) have not been veri ed. This study aimed to explore the potential mechanisms by which kaempferol regulates GA by network pharmacology and experimental validation. MethodsPotential drug targets for GA were identi ed with a protein-protein interaction network. Then, we performed a KEGG pathway analysis to elucidate the major pathway involved in the kaempferol-mediated treatment of GA. In addition, the molecular docking was performed. A rat model of GA was constructed to verify the results of network pharmacology analysis and investigate the mechanism of kaempferol against GA. ResultsThe network pharmacology study indicated that there were 275 common targets of kaempferol and GA treatment. Kaempferol exerted therapeutic effects on GA, in part, by regulating the IL-17, AGE-RAGE, p53, TNF, and FoxO signalling pathways. Molecular docking results showed that kaempferol stably docked with the core MMP9, ALB, CASP3, TNF, VEGFA, CCL2, CXCL8, AKT1, JUN and INS. Experimental validation suggested that kaempferol eased MSU-induced mechanical allodynia, ankle oedema and in ammation. It signi cantly suppressed the expression of IL-1β, IL-6, TNF-α, and TGF-β1. Kaempferol also restored IL-6induced Th17/Treg imbalance and affected RORγt and Foxp3 through IL-17 pathway. ConclusionThe present study clari es the mechanism of kaempferol against GA and provides evidence to support its clinical use.

Objective. This study aimed to determine the active ingredients of Huanglian Jiedu decoction (HLJDD) and the targets for treating dyslipidemia through network pharmacology to facilitate further application of HJJDD in the treatment of dyslipidemia. Methods. Potential drug targets for dyslipidemia were identified with a protein-protein interaction network. Gene ontology (GO) enrichment analysis and KEGG pathway analysis were performed to elucidate the biological function and major pathways involved in the HLJDD-mediated treatment of dyslipidemia. Results. This approach revealed 22 components, 234 targets of HLJDD, and 221 targets of dyslipidemia. There were 14 components and 31 common targets between HLJDD and dyslipidemia treatment. GO enrichment analysis showed that these targets were mainly associated with the response to DNA-binding transcription factor activity, lipid localization and storage, reactive oxygen species metabolic process, and inflammatory response. The results of KEGG analysis indicated that the AGE-RAGE, NF-κB, HIF-1, IL-17, TNF, FoxO, and PPAR signalling pathways were enriched in the antidyslipidemic action of HLJDD. Conclusion. This study expounded the pharmacological actions and molecular mechanisms of HLJDD in treating dyslipidemia from a holistic perspective, which may provide a scientific basis for the clinical application of HLJDD.