Icariin: A Potential Lipid Metabolism Regulator in Osteoarthritis

Abstract

Background: Icariin is a small molecule drug capable of treating osteoarthritis. Additionally, icariin is known to have an excellent ability to regulate lipid metabolism. A growing number of studies have demonstrated that lipid metabolism is related to the pathogenesis of osteoarthritis. Therefore, by regulating lipid metabolism, icariin may have a significant role in osteoarthritis. However, the molecular mechanism by which icariin regulates lipid metabolism in osteoarthritis is currently unknown. Understanding the molecular mechanism would be helpful in the treatment of osteoarthritis. Objective: This study aimed to explore the mechanism of icariin that regulated lipid metabolism in the treatment of osteoarthritis through a combination of molecular docking and network pharmacology. Methods: Firstly, potential targets for icariin were collected from the TCMSP database, Pharm Mapper, and Swiss Target Prediction Server. Targets for osteoarthritis and lipid metabolism were obtained in OMIM, DrugBank, and GeneCards databases. Common targets of icariin, osteoarthritis, and lipid metabolism were acquired by clusterProfiler R package software. We then constructed the drug-target-signaling pathway-disease network after performing GO and KEGG enrichment analyses of common targets. Finally, we performed molecular docking validation. To support our findings, a search of PubMed was performed to find relevant literature published within the last 5 years. Results: We obtained 12 targets that may be important in the regulation of lipid metabolism in osteoarthritis by icariin. Through PPI network analysis, it was determined that 5 core targets, including TNF, PTGS2, CCND1, MMP2, and ESR1, participated in this process. Molecular docking results showed that the icariin had a high affinity to the core target proteins. Relevant studies in the literature suggest that TNF, PTGS2, MMP2, and ESR1 are the core targets. Conclusion: Icariin is a potential modulator of lipid metabolism in osteoarthritis, and the molecular mechanism may be related to core targets such as TNF, PTGS2, MMP2, and ESR1.