Abstract
Coffea arabica extract (CAE) containing 48.3 ± 0.4 mg/g of chlorogenic acid and a trace amount of caffeic acid was found to alleviate photoaging activity in human skin fibroblasts. In this study, polyphenol-rich CAE was investigated for its antioxidant and antiinflammatory properties, as well as for its capability to alleviate ultraviolet B (UVB)-induced photodamage in BALB/c hairless mice. The results indicated that 500 μg/mL of CAE exhibited a reducing power of 94.7%, ferrous ion chelating activity of 46.4%, and hydroxyl radical scavenging activity of 20.3%. The CAE dose dependently reduced UVB-induced reactive oxygen species (ROS) generation in fibroblasts. Furthermore, CAE inhibited the UVB-induced expression of cyclooxygenase-2 and p-inhibitor κB, and the translocation of nuclear factor-kappa B (NF-κB) to the nucleus of fibroblasts. In addition, CAE alleviated UVB-induced photoaging and photodamage in BALB/c hairless mice by restoring the collagen content and reduced UVB-induced epidermal hyperplasia. CAE also inhibited UVB-induced NF-κB, interleukin-6, and matrix metalloproteinase-1 expression in the hairless mouse skin. The results indicated that CAE exhibits antiphotodamage activity by inhibiting UV-induced oxidative stress and inflammation. Therefore, CAE is a candidate for use in antioxidant, antiinflammatory, and antiphotodamage products.
Highlights
In recent years, the incidence of skin cancer has increased, possibly because of the depletion of the ozone layer, causing an increased exposure to solar radiation, and the use of ultraviolet (UV) tanning beds [1]
When stimulated by UV irradiation, the ubiquitination of inhibitor κB (IκB) triggers the translocation of NF-κB into the nucleus, which further increases the production of matrix metalloproteinase (MMP)-1, and subsequently, the degradation of collagen [12,13,14]
This study investigated the potential of Coffea arabica extract (CAE) to counteract ultraviolet B (UVB) irradiation-induced oxidative stress, inflammation, and photodamage in fibroblasts and hairless mice, and elucidated the associated mechanisms
Summary
The incidence of skin cancer has increased, possibly because of the depletion of the ozone layer, causing an increased exposure to solar radiation, and the use of ultraviolet (UV) tanning beds [1]. UV radiation is the most crucial factor for skin aging, or photoaging, which is characterized by wrinkling, rough skin, and hyperpigmentation [2,3]. UVB irradiation stimulates inflammation and reactive oxygen species (ROS) formation, promoting aging-related signal transduction resulting in skin damage and photoaging. ROS upregulate cyclooxygenase (COX)-2 expression to stimulate inflammation, which cause skin erythema and sunburn [7,8,9]. When stimulated by UV irradiation, the ubiquitination of IκB triggers the translocation of NF-κB into the nucleus, which further increases the production of matrix metalloproteinase (MMP)-1, and subsequently, the degradation of collagen [12,13,14]. Interleukins (ILs) and nuclear factor-kappa B (NF-κB) may induce COX-2 expression in the skin, causing skin photodamage [15]
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