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Fucoxanthin: A Safer, Anti-inflammatory Alternative to Retinol for Skin Cells

Year: 2026

Type: article

Abstract: Objective This study aimed to comprehensively compare the efficacy, safety, and underlying molecular mechanisms of fucoxanthin, a natural carotenoid, with those of retinol, the gold-standard anti-aging agent, in key skin cell models. The objective was to evaluate the potential of fucoxanthin as a safer, anti-inflammatory alternative to retinol, focusing on retinoid activity, anti-inflammatory effects, extracellular matrix synthesis, and global transcriptomic changes. Methods High-purity fucoxanthin was extracted from the diatom Phaeodactylum tricornutum and characterized using spectral analysis, HPLC, and NMR. In vitro assessments in HaCaT keratinocytes and human dermal fibroblasts (HDFs) included cytotoxicity (CCK-8 assay), gene expression of retinoid targets (RARG, RBP1), inflammatory cytokines (IL-6, IL-8, TNF-α), and extracellular matrix components (COL1A1, COL3A1, ELN) via qPCR. A comprehensive transcriptome analysis (RNA-Seq) was performed to elucidate differential pathway regulation. Results Fucoxanthin exhibited significantly lower cytotoxicity than retinol in both cell lines. It effectively upregulated RARG and RBP1 gene expression, indicating selective transcriptional activity on retinoid-related targets. Crucially, fucoxanthin potently suppressed LPS-induced pro-inflammatory cytokine expression, whereas retinol showed inconsistent inhibition and even exacerbated TNF-α expression. Conclusion Fucoxanthin functions as a high-efficacy, low-irritancy compound that shares certain functional similarities with retinol, including the modulation of retinoid-related gene expression and stimulation of collagen synthesis, while demonstrating superior safety and anti-inflammatory properties. It delivers comparable anti-aging benefits by stimulating collagen synthesis and engaging retinoid signaling, but crucially diverges from retinol by concurrently activating robust anti-inflammatory and homeostatic mechanisms.

Source: Natural Product Communications

DOI: 10.1177/1934578x261501917