Dihydrocaffeic Acid Prevents UVB-Induced Oxidative Stress Leading to the Inhibition of Apoptosis and MMP-1 Expression via p38 Signaling Pathway

Abstract

Chronic UVB exposure promotes oxidative stress, directly causes molecular damage, and induces aging-related signal transduction, leading to skin photoaging. Dihydrocaffeic acid (DHCA) is a phenolic compound with potential antioxidant capacity and is thus a promising compound for the prevention of UVB-induced skin photodamage. The aim of this study was to evaluate the antioxidant and protective effect of DHCA against oxidative stress, apoptosis, and matrix metalloproteinase (MMP) expression via the mitogen-activated protein kinase (MAPK) signaling pathway on L929 fibroblasts irradiated with UVB. DHCA exhibited high antioxidant capacity on 2,2-diphenyl-1-picrylhydrazyl (DPPH•), 2,2-azinobis-3-ethylbenzothiazoline-6-sulphonic acid (ABTS•+), and xanthine/luminol/xanthine oxidase (XOD) assays and reduced UVB-induced cell death in the neutral red assay. DHCA also modulated oxidative stress by decreasing intracellular reactive oxygen species (ROS) and extracellular hydrogen peroxide (H2O2) production, enhancing catalase (CAT) and superoxide dismutase (SOD) activities and reduced glutathione (GSH) levels. Hence, cellular damage was attenuated by DHCA, including lipid peroxidation, apoptosis/necrosis and its markers (loss of mitochondria membrane potential, DNA condensation, and cleaved caspase 9 expression), and MMP-1 expression. Furthermore, DHCA reduced the phosphorylation of MAPK p38. These findings suggest that DHCA can be used in the development of skin care products to prevent UVB-induced skin damage.

Ceria Nanoparticles Decrease UVA-Induced Fibroblast Death Through Cell Redox Regulation Leading to Cell Survival, Migration and Proliferation

“…The human skin is prone to photoaging due largely to UV-induced excessive production of ROS. The effect is compounded by a concomitant depletion of the endogenous antioxidant system ( Shindo et al, 1994 ; Gęgotek et al, 2017 ; Oliveira et al, 2019 ) as a result of oxidative damage in cellular components ( Photoaging et al, 2019 ). Our results show that pre-treatment with nanoceria decreased L929 cells UVA-induced ROS production 24 h post-irradiation; with this effect persisting even after a further dose of UVA exposure.…”

The Lipoxin Receptor/FPR2 Agonist BML-111 Protects Mouse Skin Against Ultraviolet B Radiation

“…Exposure to UV rays induces the production of ROS by keratinocytes and immune cells [31,44]. For instance, ROS activate MAPK signaling pathway leading an increase in apoptosis of skin cells [45] and activate NF-κB signaling pathway leading to an increase in pro-inflammatory cytokine production such as IL-1β, TNF-α, and IL-6 [46]. These cytokines can activate vascular endothelial cells and contribute, therefore, to the recruitment of immune cells [47,48].…”

“…In addition, activation of NF-κB also regulates gp91 phox mRNA expression further increasing ROS production and inflammation [50]. Accordingly, treatment with PDTC (a NF-κB inhibitor) [30,51] or antioxidant molecules such as naringenin [52], dihydrocaffeic acid [45], and linalool [53] reduce UVB-induced NF-κB activation and oxidative stress, indicating a loop between ROS and this signaling pathway. Moreover, when phosphorylated, p65 NF-κB subunit competes with Nrf2 for the adaptor protein CREB binding protein (CBP) [54,55].…”

Antiphotoaging Effects of 3,5‐Dicaffeoyl‐epi‐quinic Acid via Inhibition of Matrix Metalloproteinases in UVB‐Irradiated Human Keratinocytes

“…erefore, researches focused on developing MMP inhibitors as antiphotoaging agents to prevent the UVB-induced degradation of the skin collagen [24,25]. Several studies reported very promising results indicating Evidence-Based Complementary and Alternative Medicine that ameliorating the MMP overexpression is a beneficial strategy against photoaging along with scavenging the UVBinduced ROS [26,27]. Keratinocytes form the main defense mechanism of skin against UVB irradiation as UVB rays mainly affect epidermis layer.…”