Myrcene is an aromatic volatile compound that is commercially well-known as a flavor ingredient in the food industry and a fragrance in the soap and detergent industry. Given the worldwide interest in natural antiphotoaging products, we investigated the protective effects of myrcene in UVB-irradiated human dermal fibroblasts (NHDFs). NHDFs were subjected to 144[Formula: see text]mJ/cmof UVB irradiation. The expression of intracellular reactive oxygen species (ROS), matrix metalloproteinase-1 (MMP-1), MMP-3, interleukin-6 (IL-6), transforming growth factor (TGF-[Formula: see text]1) and type I procollagen were examined. We showed that myrcene decreased the production of ROS, MMP-1, MMP-3, and IL-6, and increased TGF-[Formula: see text]1 and type I procollagen secretions. Furthermore, myrcene treatment (0.1-10[Formula: see text][Formula: see text]M) dramatically reduced the activation of MAPK-related signaling molecules such as p-ERK, p-p38, and p-JNK and AP-1 including p-c-Jun and p-c-Fos. Our data indicate that myrcene has a potential protective effect on UVB-induced human skin photoaging. Therefore, myrcene might have applications in the skincare industry.
Myrciaria dubia (HBK) McVaugh (camu-camu) belongs to the family Myrtaceae. Although camu-camu has received a great deal of attention for its potential pharmacological activities, there is little information on the anti-oxidative stress and anti-inflammatory effects of camu-camu fruit in skin diseases. In the present study, we investigated the preventative effect of 70% ethanol camu-camu fruit extract against high glucose-induced human keratinocytes. High glucose-induced overproduction of reactive oxygen species (ROS) was inhibited by camu-camu fruit treatment. In response to ROS reduction, camu-camu fruit modulated the mitogen-activated protein kinases (MAPK)/activator protein-1 (AP-1), nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), and nuclear factor of activated T cells (NFAT) signaling pathways related to inflammation by downregulating the expression of proinflammatory cytokines and chemokines. Furthermore, camu-camu fruit treatment activated the expression of nuclear factor E2-related factor 2 (Nrf2) and subsequently increased the NAD(P)H:quinone oxidoreductase1 (NQO1) expression to protect keratinocytes against high-glucose-induced oxidative stress. These results indicate that camu-camu fruit is a promising material for preventing oxidative stress and skin inflammation induced by high glucose level.
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