Potential cosmeceutical applications: Anti-aging and skin-whitening activity
In 2006, Sharma and Kaur demonstrated in mouse skin, through biochemical and histopathologic evaluations, that a topical sesamol formulation was effective in preventing photodamage (such as alterations in skin integrity, lesions, ulcers) from chronic UV exposure. They suggested the merits of further testing and consideration of sesamol as an antiaging agent.7
Almost a decade later, Srisayam et al. conducted a systematic study of the antimelanogenic and skin protective activities of sesamol. They found that sesamol exhibited significant scavenging activity of the 2,2-Diphenyl-1-picrylhydrazyl hydrate radical with an IC50 value less than 14.48 mcm. The antioxidant also suppressed lipid peroxidation (IC50 value of 6.15 mcm), and displayed a whitening effect via mushroom tyrosinase inhibition as well as inhibition of cellular tyrosinase. In noting the potent antioxidant and antityrosinase activity in comparison to the positive control – kojic acid and beta-arbutin – the researchers highlighted the potential cosmeceutical applications of sesamol.8
Baek and Lee showed in 2015 that sesamol potently suppressed melanin biosynthesis by down-regulating tyrosinase activity and regulating gene expression of melanogenesis-related proteins via microphthalmia-associated transcription factor (MITF) activity modulation. They concluded that sesamol warrants attention in the cosmetic realm as a new skin-whitening agent.9
Formulation issues
Earlier that year, Geetha et al. confirmed the apoptotic characteristics of sesamol in in vitro antiproliferative and DNA-fragmentation studies in HL60 cell lines. Because of its small size, low molecular weight, and easy permeability, its viability in topical applications is considered minimal. The investigators addressed this issue by preparing sesamol-loaded solid-lipid nanoparticles, which, when applied in a cream base in mice, revealed significant retention in the skin. Its use in in vivo anticancer studies performed on tumor production induced by 12-O-tetradecanoylphorbol 13-acetate and initiated by benzo(a)pyrene in mouse epidermis resulted in the normalization of skin cancers.10