Abstract
Ultraviolet (UV) exposure causes skin photoaging leading to skin wrinkling and sagging via production of reactive oxygen species (ROS). For this reason, protection from photoaging is an important feature in cosmeceutical and dermatological products. Natural product-derived biomaterials are highly desired as future possible ingredients, because these biomaterials are often safe and effective. In this study, we aimed to characterize the skin protective activity of Pradosia mutisii, traditionally used to treat sunburn and erythema. We determined the free radical scavenging, anti-melanogenic, and moisturizing effects of a methanol extract of Pradosia mutisii (Pm-ME) in keratinocytes (HaCaT cells), melanocytes (B16F10 cells), and fibroblasts (human dermal fibroblasts (HDFs)) at non-cytotoxic concentrations. Pradosia mutisii methanol extract contains coumaric acid as a major component, and the extract exhibited protective activity against UVB- and H2O2-induced cytotoxicity. This extract also suppressed the expression of metalloproteinases (MMPs) and cyclooxygenase (COX)-2 in HaCaT cells. A reduction of Sirt-1 expression under UVB- and H2O2-treated conditions was recovered in HaCaT cells by Pm-ME. This extract displayed significant free radical scavenging activity according to the 2,2′-azino-bis (3-ethylbenzothiazoline-6-sulphonic acid) diammonium salt (ABTS) assay. The Pm-ME also upregulated the expression levels of hyaluronic acid synthase (HAS) and transglutaminase-1 (TGM-1) in HaCaT cells, indicating a putative moisturizing activity. Interestingly, the expression of collagen type 1 (Col1A1) gene and its promoter activity, as assessed by a reporter gene assay, were found to be increased in HDF and HEK293 cells. Similarly, Pm-ME helped recover collagen levels after UVB and H2O2 treatment in HDFs as well as decreased the synthesis and secretion of melanin from B16F10 melanoma cells, which may indicate a beneficial whitening cosmetic value. The p38 inhibitor SB203580 and the JNK inhibitor SP600125 suppressed MMP-9 and COX-2 expression in H2O2-treated HaCaT cells. Similarly, the ERK inhibitor U0126 inhibited HAS-2 in Pm-ME/H2O2-treated HaCaT cells. These findings suggested that inhibition of JNK and p38 and activation of ERK could be targeted by Pm-ME. Therefore, Pm-ME may exert anti-photoaging and anti-melanogenic properties via the regulation of mitogen-activated protein kinase, which could be beneficial in the cosmeceutical industry.
Highlights
Skin is the largest organ in the body, which serves as a barrier between the organism and the environment, and is responsible for maintaining skin homeostasis and determining the organism’s survival [1]
As a major UV irradiation source, UVB can lead to the production of reactive oxygen species (ROS) such as hydrogen peroxide (H2O2) via activation of ROS-generating enzymes including NADPH oxidase, xanthine oxidase, and D-amino acid oxidase [6,7,8] and the induction of skin photoaging, which leads to skin wrinkling and sagging [9,10]
Because toxicity testing to identify potential risks in humans is a necessary and critical step in both the drug and cosmetic industries [40], the cytotoxicity of P. mutisii was tested in HaCaT, B16F10, and HDF cells
Summary
Skin is the largest organ in the body, which serves as a barrier between the organism and the environment, and is responsible for maintaining skin homeostasis and determining the organism’s survival [1]. UVB is predominantly absorbed by the upper layers of skin epidermis as well as papillary dermis, while UVA penetrates to the reticular dermis with 1000 times lower efficiency at inducing various biological effects, compared to UVB [5]. Oxidative stress response has been reported to induce various cellular component damage such as cellular membrane lipids, proteins, and nucleic acids [11]. These damaged skin cells are able to initiate inflammatory responses leading to eventual damage manifested in chronically exposed skin [12]
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