In Vitro and In Vivo Studies on Protective Action of N-Phenethyl Caffeamide against Photodamage of Skin.

Yueh-Hsiung Kuo,Chien-Wen Chen,Ping Lin,Hsiu-Mei Chiang,Yin Chu,Andrzej T Slominski

doi:10.1371/journal.pone.0136777

Yueh-Hsiung Kuo, Chien-Wen Chen + Show 4 more

Open Access

https://doi.org/10.1371/journal.pone.0136777

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Journal: PloS one	Publication Date: Sep 14, 2015
Citations: 25	License type: CC BY 4.0

Affiliation: China Medical University, Asian University

Abstract

In our previous study, N-phenethyl caffeamide (K36) was proved to act as an antioxidant and an antiphotoaging agent by inhibiting type I procollagen degradation and stimulating collagen synthesis in human skin fibroblasts. In the present study, in vitro and in vivo experiments were conducted to investigate the mechanism of action and the antiinflammatory and antiphotoaging activity of K36. K36 reduced UVB-induced cyclooxygenase-2 (COX-2) and inducible nitric oxide synthases (iNOS) expression by regulating IκB and p-IκB expression. K36 also inhibited the nuclear translocation of NF-κB. Furthermore, the inhibition of mitogen-activated protein (MAP) kinases by K36 was attributed to the downregulation of COX-2. Topically applying K36 led to efficient antiwrinkle formation and reduced UVB-induced erythema and thickness of epidermis in hairless mice. In addition, K36 penetrated into the skin of hairless mice. Our findings show that K36 has significant beneficial effects on antioxidant, antiinflammatory, and antiphotoaging activity and suggest that K36 can be developed as an antiaging agent for cosmetic and skin care products.

Highlights

Overexposure to ultraviolet (UV) irradiation causes oxidative stress, inflammation, hyperpigmentation, mutation, and degradation of the extracellular matrix (ECM), resulting in wrinkling and skin cancer [1]
We previously reported that K36 exhibited antiphotodamage activity by scavenging intracellular reactive oxygen species (ROS), inhibiting the MAPK/activator protein-1 (AP-1)/MMP pathway, and alleviating UV-induced collagen decomposition in human skin fibroblasts [14]
The inducible nitric oxide synthases (iNOS) expression was reduced after K36 treatment in a dose-dependent manner

Summary

Introduction

Overexposure to ultraviolet (UV) irradiation causes oxidative stress, inflammation, hyperpigmentation, mutation, and degradation of the extracellular matrix (ECM), resulting in wrinkling and skin cancer [1]. UV irradiation generates reactive oxygen species (ROS), triggering signal transduction cascades and activating inflammatory cytokines [2, 3]. These cytokines subsequently activate protein kinases, such as the mitogen-activated protein kinases (MAP kinases) and regulate downstream transcription factors [e.g., cyclooxygenase-2 (COX-2) and nuclear factor-κB (NF-κB)] causing an inflammatory response [4]. UVB irradiation increases the activity levels of phospholipase A2 and COX-2, resulting in inflammation, erythema, and related symptoms of the skin [6].

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