Abstract

The potential protective effect of nanoliposomes loaded with lotus seedpod oligomeric procyanidin (LSOPC) against melanogenesis and skin damaging was investigated. Fluorescence spectroscopy showed that, after encapsulation, the LSOPC-nanoliposomes still possessed strong inhibitory effects against melanogenesis, reducing the activity of both monophenolase and diphenolase. Molecular docking indicated that LSOPC could generate intense interactive configuration with tyrosinase through arene–H, arene–arene, and hydrophobic interaction. An ultraviolet radiated cell-culture model (human foreskin fibroblast cell (HFF-1)) was used to determine the protective effects of the LSOPC-nanoliposomes against skin aging and damage. Results showed that LSOPC-nanoliposomes exerted the highest protective effects against both ultraviolet B (UVB) and ultraviolet A (UVA) irradiation groups compared with non-encapsulated LSOPC and a control (vitamin C). Superoxide dismutase (SOD) and malonaldehyde (MDA) assays demonstrated the protection mechanism may be related to the anti-photooxidation activity of the procyanidin. Furthermore, a hydroxyproline assay suggested that the LSOPC-nanoliposomes had a strong protective effect against collagen degradation and/or synthesis after UVA irradiation.

Highlights

  • The skin is the outermost physical barrier protecting humans from external injuries [1]

  • Gas chromatography was used to determine the presence of any residual organic solvents in the lotus seedpod oligomeric procyanidin (LSOPC)-nanoliposomes after their fabrication

  • The IC50 of the LSOPC-nanoliposomes (256.1 ± 7.2 μg/mL) was slightly smaller than that of the LSOPC (265.2 ± 5.2 μg/mL), which suggests that encapsulation somewhat facilitated the interaction of LSOPC with l-DOPA. These results show that the LSOPC-nanoliposomes possessed a higher affinity for the melanogenesis substrates than free LSOPC, which may indicate a higher preventive effect against skin spots

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Summary

Introduction

The skin is the outermost physical barrier protecting humans from external injuries [1]. Sunlight induces the formation of electrons (e-) and holes (h+), whose interactions lead to the accumulation of reactive oxygen species (ROS), including superoxide anion radical (O2− ), singlet oxygen (1 O2 ), and hydroxyl radicals (OH), etc. High levels of ROS give rise to various skin damages, such as inflammation, wrinkling, discoloration, and erythema/edema [3]. The ultraviolet (UV) radiation in sunlight is believed to be the main cause of these adverse effects. The brownish polymer melanin in skin is produced in melanocytes, located on the basal layer between the dermis and epidermis. The type, amount, and distribution of melanin determines skin color. Melanin functions in humans similar to polyphenols, absorbing UV sunlight and removing

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