Abstract

Opuntia humifusa is a type of cactus whose fruits have been used in folk medicine for the treatment of several diseases. In the present study, we aimed to determine whether O. humifusa fruit water extract (OHE) has inhibitory effects against solar ultraviolet (sUV)-induced matrix metalloproteinase-1 (MMP-1) expression. In ex vivo human skin, we found that OHE suppressed sUV radiation-induced MMP-1 expression. The inhibitory effect of OHE was confirmed in human dermal fibroblasts. OHE treatment reduced sUV-induced MMP-1 expression by suppressing reactive oxygen species (ROS) generation and phosphorylation of c-Jun, a component of transcription factor activator protein 1 (AP-1). On the other hand, OHE recovered the tissue inhibitor of matrix metalloproteinase 1 (TIMP-1) and type 1 collagen production attenuated by sUV. As upstream signaling pathways for AP-1, MKK4-JNK, MEK-ERK, and MKK3/6-p38 phosphorylation were downregulated by OHE treatment. In addition, OHE exhibited DPPH radical scavenging activity. These findings demonstrate that OHE has a preventive effect against sUV-induced skin damage via suppression of pathways triggered by ROS.

Highlights

  • Human skin is in direct contact with the environment and undergoes aging as a consequence of environmental damage

  • The increased activation of activator protein 1 (AP-1) is involved in the degradation of collagen via inducing matrix metalloproteinase (MMP) production, which leads to alteration of the extracellular matrix (ECM) in skin [8]

  • We investigated whether O. humifusa fruit water extract (OHE) can promote an anti-photoaging effect in solar ultraviolet (sUV) radiated primary human dermal fibroblasts (HDFs) by analyzing the expression of matrix metalloproteinase-1 (MMP-1) and collagen, and the underlying signal pathway(s) involved

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Summary

Introduction

Human skin is in direct contact with the environment and undergoes aging as a consequence of environmental damage. The primary environmental factor that causes human skin aging is ultraviolet (UV) radiation, and repeated exposure to UV causes premature skin aging (photoaging) [1,2]. UV radiation-induced ROS production, in turn, activates the mitogen-activated protein kinase (MAPK) signaling cascades, which consist of extracellular signal-regulated kinases (ERK), p38 MAPK, and c-Jun N-terminal kinases (JNK) that induce subsequent activation of transcription factor activator protein 1 (AP-1) [6]. The increased activation of AP-1 is involved in the degradation of collagen via inducing matrix metalloproteinase (MMP) production, which leads to alteration of the extracellular matrix (ECM) in skin [8]. MMP-1 plays an important role in the process of photoaging because it cleaves the type 1 collagen, which is the most abundant protein in skin connective tissue [8,9]

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