Abstract: In this study, the ingredient targets of astaxanthin were predicted by Pharm mapper databases, and the targets of breast cancerwere obtained by OMIM-Online Mendelian Inheritance in Man (OMIM) and Therapeutic Target Database(TTD); the direct target was ob-tained through intersection of astaxanthin targets and breast cancer targets, and the software of Cytoscape 3. 7. 1 was used to construct the pro-tein-protein interaction networks of key targets; enrichment of gene function and pathways of all potential targets was conducted by Gene On-tology(GO)database and Kyoto Encyclopedia of Genes and Genomes(KEGG)database to explore the mechanism of astaxanthin for the inhibi-tion of breast cancer. MTT was used to detectcell proliferation. The expression ofp-AKT and PI3K was tested by Western Blot. There were 21targets of astaxanthin inhibiting breast cancer and three core targets (ADIPOQ, BECNI and PGR). These targets were participated in critical pathway such as cancer pathway, immune system and cytokines to inhibit breast cancer. ASX of 150 and 300 μmol / L significantly inhibited the growth of breast cancer 4T1 cells. ASX could significantly reduce the phosphorylation of AKT and the expression level of PI3K. There-fore, it was induced that astaxanthin could prevente breast cancer through the PI3K/ AKT signaling pathway.

Key words: astaxanthin, breast cancer, inhibition, network pharmacology, molecular mechanism