Abstract:
Calendula officinalis (marigold) has long been valued in traditional medicine for its therapeutic effects, yet the molecular mechanisms underlying its action remain largely unexplored. This study investigates the bioactive phytochemicals of marigold and their potential role in treating cancer and non-alcoholic fatty liver disease (NAFLD), using computational analysis of publicly available RNA-sequencing datasets. Five major compounds - Lutein, and Lycopene, Vitamin E, Fucoxanthin, and Quercetin were selected for detailed analysis. The workflow involved quality control, alignment to species-specific reference genomes, differential gene expression analysis using DESeq2, and functional enrichment via KEGG pathways and Gene Ontology. Lycopene was found to influence genes involved in lipid metabolism and inflammation, with dysregulation of SQLE, PNPLA3, PFKFB3, IL10, SIRT7, COL1A1, and ACTA2, to name a few. Vitamin E affected insulin and MAPK signaling pathways, leading to changes in GATA3, PNPLA3, SREBF2, IL6, and CD36. Fucoxanthin modulated metabolic and inflammatory processes through genes such as ISG15, FDFT1, and PCSK9. Quercetin demonstrated strong antioxidant and anti-inflammatory potential by altering the expression of SOD2, CAT, TNF, NOX1, and Smad4. Lutein influenced cancer-associated pathways like PI3K/AKT and apoptosis, with dysregulation of GATA3, ING3, TES, PCK2, and PELP1. While many of the gene expression changes suggest therapeutic benefit, certain observations - particularly involving Vitamin E and Lycopene, indicate complex responses that warrant further functional validation. Overall, this study offers molecular insights into the mechanisms underlying the traditional use of marigold and supports the potential of its phytochemicals as plant-based therapeutics for complex diseases such as cancer and NAFLD.