Abstract
Quercetin is a naturally occurring polyphenol present in various fruits and vegetables. The bioactive properties of quercetin include anti-oxidative, anti-cancer, anti-inflammatory, and anti-diabetic effects. However, the effect of quercetin on skin aging and the direct molecular targets responsible have remained largely unknown. Herein, we investigated the protective effect of quercetin against UV-mediated skin aging and the molecular mechanisms responsible. Treatment with quercetin suppressed UV-induced matrix metalloproteinase-1 (MMP-1) and cyclooxygenase-2 (COX-2) expression and prevented UV-mediated collagen degradation in human skin tissues. Quercetin exerted potent inhibitory effects towards UV-induced activator protein-1 (AP-1) and nuclear factor-kappa B (NF-κB) activity. Further examination of the upstream signaling pathways revealed that quercetin can attenuate UV-mediated phosphorylation of extracellular signal-regulated kinase (ERK), c-Jun N terminal kinases (JNK), protein kinase B (Akt), and signal transducer and activator of transcription 3 (STAT3). Kinase assays using purified protein demonstrated that quercetin can directly inhibit protein kinase C delta (PKCδ) and Janus kinase 2 (JAK2) kinase activity. Quercetin was observed to bind to PKCδ and JAK2 in pull-down assays. These findings suggest that quercetin can directly target PKCδ and JAK2 in the skin to elicit protective effects against UV-mediated skin aging and inflammation. Our results highlight the potential use of quercetin as a natural agent for anti-skin aging applications.
Highlights
The process of skin aging involves both endogenous and exogenous aging and is generally associated with deep wrinkles, pigmentation, sagging, and laxity [1,2]
Exposure to UV induces the activation of Protein kinase C (PKC) family members including PKC-delta (PKCδ), which in turn interact with the mitogen-activated protein kinase (MAPK) pathways [7,8]
Because UV mediates skin aging through promoting inflammatory responses, we evaluated the effects of quercetin on Cyclooxygenase 2 (COX-2) expression, a major inducer of inflammation [5]
Summary
The process of skin aging involves both endogenous and exogenous aging and is generally associated with deep wrinkles, pigmentation, sagging, and laxity [1,2]. Exposure to UV induces the activation of Protein kinase C (PKC) family members including PKC-delta (PKCδ), which in turn interact with the mitogen-activated protein kinase (MAPK) pathways [7,8]. Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT-3) signaling pathway plays a critical role in skin inflammation [12,13]. These studies provide evidence that PKCδ and JAK2 act as key intermediates in UV-mediated signaling, and the potential to be therapeutic targets in preventing skin-aging. Quercetin (3,3 ,4 ,5,7-pentahydroxyflavone), a well-known member of the flavonoid family, has been reported to elicit a variety of beneficial effects, including anti-oxidant, anti-inflammatory, and anti-carcinogenic activities [14,15]. We sought to investigate the mechanisms of action responsible for the effects of quercetin against UV-induced skin aging in skin cells and human skin tissue
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