The effect of passion fruit, the fruit of Passiflora edulis , on melanin inhibition and collagen synthesis was studied using cultured human melanoma and fibroblast cells. Passion fruit was divided into three parts, rind (PF-R), pulp (PF-P), and seed (PF-S), and each part was extracted using 80% ethanol. The concentration of polyphenols was higher in PF-S than in PF-R or PF-P. Treatment of melanoma cells with PF-S led to inhibition of melanogenesis. In addition, the production of total soluble collagen was elevated in dermal fibroblast cells cultured in the presence of PF-S. PF-R and PF-P did not yield these effects. Furthermore, the removal of polyphenols from PF-S led to the abolishment of the effects described above. We discovered that piceatannol (3,4,3',5'-tetrahydroxy-trans-stilbene) is present in passion fruit seeds in large amounts and that this compound is the major component responsible for the PF-S effects observed on melanogenesis and collagen synthesis.

Piceatannol is present in passion fruit (Passiflora edulis) seeds in high amounts. In this study, we isolated the second major polyphenolic compound of passion fruit seeds and identified it as scirpusin B, which is a dimer of piceatannol. We investigated the antioxidant activities and vasorelaxing effects of these polyphenols. Their antioxidant effects were measured using an in vitro 1,1-diphenyl-2-picrylhydrazyl (DPPH) radical scavenging assay, and their vasorelaxant effects were determined ex vivo in rat thoracic aorta. Both polyphenolic compounds exhibited potent antioxidant activities and significant vasorelaxant effects in endothelium-intact aortas. More specifically, scirpusin B exerted a greater antioxidant activity and vasorelaxant effect compared with that of piceatannol. Additionally, the vasorelaxation effects of the compounds were induced via the NO derived from the endothelium. This study provides the possibility that polyphenols in passion fruit seeds are effective against cardiovascular diseases (CVDs).

The use of naturally occurring botanicals with substantial antioxidant activity to prevent photoageing is receiving increasing attention. We have previously identified piceatannol and scirpusin B, which is a dimer of piceatannol, as strong antioxidants that are present in passion fruit (Passiflora edulis) seeds. In the present study, the effects of passion fruit seed extract, piceatannol, and scirpusin B on human keratinocytes were investigated. The passion fruit seed extract and piceatannol upregulated the glutathione (GSH) levels in keratinocytes in a dose-dependent manner, indicating that piceatannol is an active component of the passion fruit seed extract in keratinocytes. The pretreatment with piceatannol also supressed the UVB-induced generation of reactive oxygen species (ROS) in the keratinocytes. In addition, the transfer of the medium from the UVBirradiated keratinocytes to non-irradiated fibroblasts enhanced matrix-metalloproteinase (MMP)-1 activity, and this MMP-1 induction was reduced when the keratinocytes were pretreated with piceatannol. These results suggest that piceatannol attenuates the UVB-induced activity of MMP-1 along with a reduction of ROS generation in keratinocytes. Thus, piceatannol and passion fruit seed extract containing high amounts of piceatannol are potential anti-photoageing cosmetic ingredients.Key words piceatannol; passion fruit seed; keratinocyte; ultraviolet; reactive oxygen species; matrix-metalloproteinase Solar UV irradiation damages human skin causing it to age prematurely, a process referred to as photoageing, and to develop the characteristics of thickened epidermis and increased melanogenesis.1-3) In contrast, intrinsic (chronological) ageing is characterised by skin atrophy accompanied by a loss of elasticity and reduced metabolic activity. [4][5][6][7][8] A hallmark of photoageing is the disorganisation of collagen, the major structural component of the skin. Collagen is produced mainly by dermal fibroblasts and is degraded by the matrix metalloproteinases (MMPs) that are secreted by various cells, including keratinocytes, fibroblasts, and inflammatory cells.2,8,9) UV irradiation, particularly UVB (290-320 nm) and UVA (315-400 nm), induces the expression of matrix metalloproteinase-1 (MMP-1) in the fibroblasts, which is mainly responsible for the degradation of the dermal collagen in the ageing process of human skin. Therefore, UV-induced MMP-1 is considered to contribute substantially to the connective tissue damage that causes severe collagen deficiency and wrinkling during photoageing.2,8) Although keratinocytes do not produce MMP-1 in response to UVB irradiation, damaged epidermal keratinocytes indirectly play important roles in the release of MMP-1. It has been reported that the culture medium of UVB-irradiated keratinocytes stimulates MMP-1 release from fibroblasts more efficiently than the direct irradiation of the fibroblasts. 10,11)The primary mechanism by which UV irradiation initiates molecular responses in human skin is through the photochromic genera...

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