Effect of ferulic acid and p-coumaric acid on lowering uric acid through network pharmacology and in vitro studies

Abstract

The occurrence of hyperuricemia is increasing yearly. Based on network pharmacology, this study predicted the molecular targets and signaling pathways of ferulic acid and p-coumaric acid for improving hyperuricemia. The results were verified through in vitro cell experiments. After enrichment analysis of 11 core targets of ferulic acid and p-coumaric acid to improve hyperuricemia, the phosphatidylinositol 3 kinase/protein kinase B (PI3K/Akt) signaling pathway was considered as the most significant signaling pathway. In the hyperuricemia cell model, ferulic acid and p-coumaric acid significantly increased cell viability and decreased the cell uric acid (UA) content. Ferulic acid and p-coumaric acid significantly regulated the expression of UA transport-related proteins, namely urate organic anion transporter 1, glucose transporter 9, and adenosine triphosphate-binding transporter protein G2. Ferulic acid and p-coumaric acid also downregulated the phosphorylation of PI3K and Akt, which inhibited the PI3K/Akt signaling pathway. This study confirmed that ferulic acid and p-coumaric acid could regulate UA-related proteins through the PI3K/Akt pathway and promote UA excretion to alleviate hyperuricemia. The results of this research provided a theoretical basis for further research and development of UA-lowering products.