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<p>Photoaging, a premature skin aging caused by exposure to UVA radiation, is a significant dermatological problem driven by oxidative stress and inflammatory responses. The radio-resistant extremophile <i>Deinococcus radiodurans</i> is the source of the oxy-carotenoid Deinoxanthin, which has emerged as a noteworthy antioxidant with possible photoaging therapeutic uses. This investigation employed an integrated network pharmacology analysis to explain the possible molecular targets and biological mechanisms of deinoxanthin toward photoaging. Intersection analysis between deinoxanthin-related and photoaging-related targets showed 47 overlapping targets, suggesting potential molecular candidates for exploring deinoxanthin therapeutic efficacy. The protein-protein interaction network was built from these targets and identified eight core targets: TNF-α, PPARG, IL-6, NFκB1, MAPK3, CASP3, EGFR, and ESR1. Docking analysis exhibited strong binding affinities of DRE with the top three core targets: TNF-α, MAPK3, and NFκB1. The dynamics simulation and binding free energy study with over 100 nanoseconds further decoded the stability of deinoxanthin-MAPK3 and deinoxanthin-TNF-α complexes, showing stable conformations, while the deinoxanthin-NFκB1 complex showed significant fluctuations, indicating potential instability. Cytotoxicity assays confirm that Deinoxanthin-rich extract (DRE) concentrations up to 15&#xa0;µg/mL did not harm NIH/3T3 cells. Western blot analysis further confirmed that the DRE pre-treatment significantly reduced upregulated TNF-α, MAPK3, and NFκB1 levels in UVA-exposed cells, showcasing its protective effects towards photoaging by modulating signaling pathways and inhibiting oxidative stress.</p>

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Photoprotective effects of deinoxanthin against UVA-Induced oxidative damage: an integrative computational and cellular analysis

  • 期刊论文

  • 发表日期：

    2026年1月14日

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  • Karankumar Balamurugan,
  • Antony Stalin,
  • Charan Singh Pawar,
  • N. Rajendra Prasad

摘要

Photoaging, a premature skin aging caused by exposure to UVA radiation, is a significant dermatological problem driven by oxidative stress and inflammatory responses. The radio-resistant extremophile Deinococcus radiodurans is the source of the oxy-carotenoid Deinoxanthin, which has emerged as a noteworthy antioxidant with possible photoaging therapeutic uses. This investigation employed an integrated network pharmacology analysis to explain the possible molecular targets and biological mechanisms of deinoxanthin toward photoaging. Intersection analysis between deinoxanthin-related and photoaging-related targets showed 47 overlapping targets, suggesting potential molecular candidates for exploring deinoxanthin therapeutic efficacy. The protein-protein interaction network was built from these targets and identified eight core targets: TNF-α, PPARG, IL-6, NFκB1, MAPK3, CASP3, EGFR, and ESR1. Docking analysis exhibited strong binding affinities of DRE with the top three core targets: TNF-α, MAPK3, and NFκB1. The dynamics simulation and binding free energy study with over 100 nanoseconds further decoded the stability of deinoxanthin-MAPK3 and deinoxanthin-TNF-α complexes, showing stable conformations, while the deinoxanthin-NFκB1 complex showed significant fluctuations, indicating potential instability. Cytotoxicity assays confirm that Deinoxanthin-rich extract (DRE) concentrations up to 15 µg/mL did not harm NIH/3T3 cells. Western blot analysis further confirmed that the DRE pre-treatment significantly reduced upregulated TNF-α, MAPK3, and NFκB1 levels in UVA-exposed cells, showcasing its protective effects towards photoaging by modulating signaling pathways and inhibiting oxidative stress.