Based on network pharmacology, molecular docking technology, and cell experiments, this study explores the role and potential mechanisms of icariin (ICA) in delaying skin photoaging. The SwissTargetPrediction and GeneCard databases were used to screen for potential targets of ICA. Skin photoaging-related targets were obtained through the OMIM and DrugBank databases. The common targets between these two sets were imported into the STRING database for analysis and a protein interaction network was constructed using Cytoscape 3.7.2 software. Further, the DAVID database was used for gene ontology (GO) and kyoto encyclopedia of genes and genomes (KEGG) enrichment analyses to identify key signaling pathways. Molecular docking of ICA with core targets was performed using AutoDock 4.2.6 software. Finally, cell experiments were conducted to validate the key targets. Network pharmacology analysis identified 123 potential targets related to skin photoaging, with 10 key core targets, including B-cell lymphoma 2 (BCL-2) and cysteinyl aspartate specific protease-3 (Caspase-3). GO and KEGG enrichment analyses showed that these targets are mainly involved in signaling pathways such as phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT). Molecular docking results indicated that ICA has strong binding activity with BCL-2 and Caspase-3. Cell experimental results demonstrated that ICA significantly inhibits the aging and apoptosis of HaCaT cells. Moreover, compared with the ultraviolet B (UVB) group, in the ICA group, the protein expression levels of BCL-2-associated X protein (BAX) and Cleaved Caspase-3 were decreased, while the protein expression levels of phosphorylated PI3K (p-PI3K), phosphorylated AKT (p-AKT), and BCL-2 were significantly increased. In summary, ICA delays skin photoaging by regulating the PI3K/AKT signaling pathway to inhibit cell apoptosis.