Mechanism of icariin in delaying skin photoaging based on network pharmacology and experimental verification – Raw data

Construct a protein interaction network using Cytoscape 3.7.2 software. Further use the DAVID database for GO and KEGG enrichment analysis to identify their key signaling pathways. Verify the docking between ICA and core targets using AutoDock 4.2.6 software.

Finally, the key targets were validated through cell experiments. According to network pharmacology analysis, there are a total of 123 potential targets associated with ICA and skin photoaging, including 10 key core targets, including B-cell lymphoma-2 (BCL-2) and cysteine aspartate specific protease-3 (Caspase-3). GO and KEGG enrichment analysis showed that these targets mainly involve signaling pathways such as phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT).

The molecular docking results showed that ICA has strong binding activity with target BCL-2 and Caspase-3. The cell experiment results showed that ICA can significantly inhibit the aging and apoptosis of HaCaT cells. In addition, compared with the ultraviolet B (UVB) group, the ICA group showed a decrease in the expression levels of BCL-2-associated X protein (BAX) and cleaved Caspase-3 protein, while the expression levels of phosphorylated PI3K (p-PI3K), phosphorylated AKT (p-AKT), and BCL-2 protein were significantly increased.

In summary, ICA inhibits cell apoptosis and delays skin photoaging by regulating the PI3K/AKT signaling pathway.