Abstract
Ultraviolet B (UVB) irradiation is viewed as the principal inducer of skin photo-aging, associated with acceleration of collagen degradation and upregulation of matrix metalloproteinases (MMPs). The ethnic groups of southern/western China use Fuzhuan brick-tea (FBT) as a beverage and as a nutritional supplement. In this study, we scrutinized the antagonistic effects of aqueous extract of Fuzhuan-brick tea (FBTA) on skin photo-aging in UVB-exposed human keratinocyte (HaCaT) cells. FBTA exhibited strong antioxidant activity and quenched UVB-induced generation of cellular reactive oxygen species (ROS) without showing any toxicity. FBTA was capable of combating oxidative stress by augmenting messenger RNA (mRNA) and protein levels of both phase I and phase II detoxifying enzymes, especially heme oxygenase 1 (HO-1), by upregulating the nuclear factor erythroid 2-related factor 2 (Nrf2)-mediated pathway in HaCaT cells via the phosphorylation of p38 and extracellular signal-regulated kinase (ERK). FBTA also downregulated the expression of matrix metalloproteinase-1 (MMP-1) while upregulating type I procollagen by modulating Nrf2 signaling in UVB-irradiated HaCaT cells. Collectively, our results show that FBTA might be useful as a functional food while being a good candidate in the development of cosmetic products and medicines for the remedy of UVB-induced skin photo-aging.
Highlights
Ultraviolet (UV) irradiation is viewed as one of the main factors causing structural and functional alterations in the skin, triggering skin aging [1]
Gallic acid remarkably elevated type 1 procollagen levels in Ultraviolet B (UVB)-stimulated cells (Figure 7A). These findings suggest that Fuzhuan-brick tea (FBTA) could prevent UVB-induced photoaging by lessening the matrix metalloproteinases (MMPs)-1 upregulation and type I procollagen downregulation in skin keratinocytes, probably due to the presence of gallic acid, because during the permeation process, galloyl-catechins are metabolized by skin esterase and produce more gallic acid in the skin [27]
Our findings revealed for the first time that FBTA pretreatment mitigated UVB-induced photoaging in human keratinocyte HaCaT cells (Figure 8)
Summary
Ultraviolet (UV) irradiation is viewed as one of the main factors causing structural and functional alterations in the skin, triggering skin aging [1]. Accumulating evidences show that skin photo-aging induced by UV-irradiation is associated with either excessive production of reactive oxygen species (ROS) or inflammatory mediators and disturbance of extracellular matrix (ECM) proteins [2,3]. UVB-stimulated redundant formation of intracellular ROS can cause an imbalance of cellular oxygen levels, triggering oxidative stress and impairing the antioxidant defense system, causing of photo-aging [4]. ROS boost the production of matrix metalloproteinases (MMPs) which can enhance the degradation of ECM proteins such as collagen and elastin, which are the foremost structural proteins in skin connective tissue, thereby leading to skin photo-aging [5,6].
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