JOURNALS

Our skin is constantly exposed to blue light (BL), which is abundant in sunlight and emitted by digital devices. Prolonged exposure to BL can lead to oxidative stress-induced damages and skin hyperpigmentation. For this study, we used a cell line-based model to examine the protective effects of tocotrienol-rich fraction (TRF) on BL-induced oxidative stress and hyperpigmentation in B16-F1 melanocytes. Alpha-tocopherol (αTP) was used as a comparator. Molecular assays such as cell viability assay, flow cytometry, western blotting, fluorescence imaging, melanin and tyrosinase analysis were performed. Our results showed that TRF effectively suppressed the formation of reactive oxygen species and preserved the mitochondrial membrane potential. Additionally, TRF exhibited anti-apoptotic properties by reducing the activation of the p38 mitogen-activated protein kinase molecule and downregulating the expression of cleaved caspase-3. Moreover, TRF modulated tyrosinase activity, resulting in a lowered rate of melanogenesis and reduced melanin production. In contrast, αTP did not exhibit significant protective effects against skin damages and pigmentation in BL-induced B16-F1 cells. Therefore, this study indicates that TRF may offer superior protective effects over αTP against the effects of BL on melanocytes. These findings demonstrate the potential of TRF as a protective natural ingredient that acts against BL-induced skin damages and hyperpigmentation via its anti-oxidative and anti-melanogenic properties.

Urban particulate matter (PM) is a major air pollutant that triggers molecular processes and is detrimental to the skin. We investigated the protective effects of tocotrienol-rich fraction (TRF) against urban PM-induced skin ageing, inflammation, and skin barrier dysfunction in human epidermal keratinocytes. Alpha-tocopherol (αTP) and retinoic acid (RA) were used as comparators. Our results showed that TRF significantly restored cell viability and alleviated increased intracellular reactive oxygen radicals in PM-treated keratinocytes. In addition, TRF significantly downregulated the activation of mitogen-activated protein kinases in PM-stimulated keratinocytes. This was substantiated by lower protein expression in the phosphorylation of extracellular signal-regulated kinase, Jun N-terminal kinase, and p38. This resulted in the inhibition of cyclooxygenase-2 expression, which is a downstream inflammatory mediator. TRF significantly protected skin barrier function upon exposure to PM by upregulating filaggrin, transglutaminase-1, and involucrin. In contrast, αTP and RA did not exhibit protective effects against skin damages in the PM-treated keratinocytes. Overall, this study suggests that TRF possesses antioxidant, anti-inflammatory, and skin barrier protective properties, and may serve as a potential ingredient in personal care and cosmeceutical industries to combat skin damage due to air pollution.

Background: Oxidative stress and inflammation are some of the proposed mechanisms involved in the pathogenesis of atopic dermatitis (AD). Current pharmacotherapeutic approaches are effective yet they are not without adverse effects. Vitamin E has great potential as an adjunctive treatment for AD owing to its antioxidant and anti-inflammatory bioactivities.

Summary: This review article summarizes the current available evidence from cellular, animal and clinical studies on the relationship between vitamin E and AD. The future prospects of vitamin E are also discussed. Vitamin E in practice does not show any toxicity to humans within a range of reasonable dosage. Albeit rarely, vitamin E as a contact allergen should be considered. Collectively, this review envisaged vitamin E as an adjunctive treatment for AD patients. Future research on the distinct effects of different vitamin E isoforms as well as their delivery system in skin disorders is needed.