Abstract
Xeroderma pigmentosum (XP) is a rare autosomal recessive hereditary disorder. As patients with XP are deficient in nucleotide excision repair, they show severe photosensitivity symptoms. Although skin protection from ultraviolet (UV) radiation is essential to improve the life expectancy of such patients, the optimal protective effect is not achieved even with sunscreen application, owing to the low usability of the preparations. Nanosheets are two-dimensional nanostructures with a thickness in the nanometer range. The extremely large aspect ratios of the nanosheets result in high transparency, flexibility, and adhesiveness. Moreover, their high moisture permeability enables their application to any area of the skin for a long time. We fabricated preparations containing avobenzone (BMDBM) based on freestanding poly (L-lactic acid) (PLLA) nanosheets through a spin-coating process. Although monolayered PLLA nanosheets did not contain enough BMDBM to protect against UV radiation, the layered nanosheets, consisting of five discrete BMDBM nanosheets, showed high UV absorbance without lowering the adhesive strength against skin. Inflammatory reactions in XPA-deficient mice after UV radiation were completely suppressed by the application of BMDBM-layered nanosheets to the skin. Thus, the BMDBM layered nanosheet could serve as a potential sunscreen preparation to improve the quality of life of patients with XP.
Highlights
Xeroderma pigmentosum (XP) is a rare autosomal recessive hereditary disorder characterized by severe photosensitive and neurological symptoms [1–3]
XP are deficient in nucleotide excision repair (NER) for DNA lesions induced by ultraviolet (UV) radiation [4]
We previously reported that freestanding nanosheets composed of biodegradable and biocompatible polymers, such as poly and poly acid, are promising vehicles for topical and transdermal drug delivery systems [22]
Summary
Xeroderma pigmentosum (XP) is a rare autosomal recessive hereditary disorder characterized by severe photosensitive and neurological symptoms [1–3]. XP are deficient in nucleotide excision repair (NER) for DNA lesions induced by ultraviolet (UV) radiation [4]. This results in increased photosensitivity, leading to severe sunburn, freckling, xerosis, progressive development of pigmentation, and cancer in the sun-exposed area of the skin. Patients with XP often display skin cancer starting from early childhood, ocular diseases such as photophobia, and fetal neurodegeneration. The median age at death is 32 years, and 60% of premature deaths are caused by skin cancer [5]. XP is classified into eight subtypes by genetic mutation: NER-deficient types (XP-A to G) and variant type (XP-V), in which translesion DNA synthesis is impaired [6].
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