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. 2017 Apr 7;18(4):782.
doi: 10.3390/ijms18040782.

Alleviation of Ultraviolet B-Induced Photodamage by Coffea arabica Extract in Human Skin Fibroblasts and Hairless Mouse Skin

Po-Yuan Wu  1   2 , Chi-Chang Huang  3 , Yin Chu  4 , Ya-Han Huang  5 , Ping Lin  6 , Yu-Han Liu  7 , Kuo-Ching Wen  8 , Chien-Yih Lin  9 , Mei-Chich Hsu  10 , Hsiu-Mei Chiang  11
Affiliations

Alleviation of Ultraviolet B-Induced Photodamage by Coffea arabica Extract in Human Skin Fibroblasts and Hairless Mouse Skin

Po-Yuan Wu et al. Int J Mol Sci. .

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.

Keywords: Coffea arabica; antioxidant; inflammatory; inhibitor κB (IκB); nuclear factor-kappa B (NF-κB); photodamage.

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Conflict of interest statement

The authors state no conflicts of interest.

Figures

Figure 1
Figure 1
Reducing capability of CAE. Ascorbic acid (100 μg/mL) was used as the positive control. The reducing capability of CAE at concentrations above 100 μg/mL was similar to that of ascorbic acid. Significant difference versus control in each experiment: ***, p < 0.001.
Figure 2
Figure 2
Ferrous ion chelating activity of CAE. EDTA (500 μg/mL) was applied as the positive control. A significant difference between this activity and that of the untreated (0 μg/mL CAE) group could be observed. Significant difference versus control in each experiment: ***, p < 0.001.
Figure 3
Figure 3
Hydroxyl radical scavenging activity (%) of CAE. Mannitol (2500 μg/mL) was used as the positive control. CAE exhibited powerful hydroxyl radical scavenging activity. Significant difference versus control in each experiment: ***, p < 0.001.
Figure 4
Figure 4
Superoxide anion scavenging activity (%) of CAE. BHT (250 μg/mL) was used as the positive control. The superoxide anion scavenging activity of 1 and 5 μg/mL CAE was similar to that of BHT. Significant difference versus control in each experiment: ***, p < 0.001.
Figure 5
Figure 5
Hydrogen peroxide scavenging activity (%) of CAE. A significant difference between this activity and that of the untreated (0 μg/mL CAE) group can be observed. Significant difference versus control in each experiment: *, p < 0.05, ***, p < 0.001.
Figure 6
Figure 6
Examination of CAE inhibition of intracellular ROS generation in human skin fibroblasts by using a DCFH-DA assay (magnification factor: 200×). UVB irradiation increased ROS generation, whereas CAE inhibited ROS generation.
Figure 7
Figure 7
Effects of CAE on CAT activity in human skin fibroblasts. UVB irradiation inhibited CAT activity, whereas CAE treatment reversed the effect. Significant difference versus control: #, p < 0.05; significant difference versus the UVB-induced group: *, p < 0.05.
Figure 8
Figure 8
Effects of CAE on UVB-induced COX-2 expression in human skin fibroblasts. Significant difference versus control: ###, p < 0.001; significant difference versus the UVB-induced group: ***, p < 0.001.
Figure 9
Figure 9
Effect of CAE on UVB-mediated p-IκBα and IκBα expression in human skin fibroblasts. Significant difference versus control: ###, p < 0.001; significant difference versus the UVB-induced group: **, p < 0.01, ***, p < 0.001.
Figure 10
Figure 10
Effects of CAE on UVB-induced activation of NF-κB in human skin fibroblasts (magnification factor: 200×). UVB promoted the translocation of NF-κB in the nucleus and CAE inhibited this effect.
Figure 11
Figure 11
Effects of CAE on a* values in UVB-irradiated hairless mice in the tenth week. Significant difference versus the UVB-induced group: *, p < 0.05, **, p < 0.01.
Figure 12
Figure 12
Effects of CAE on TEWL in chronic UVB-irradiated hairless mice. Significant difference versus control: ###, p < 0.001; significant difference versus the UVB-induced group: ***, p < 0.001.
Figure 13
Figure 13
Photographs of wrinkles induced by UVB irradiation and the effect of topical application of CAE.
Figure 14
Figure 14
Light micrographs of the histological sections of hairless mice stained with H & E.
Figure 15
Figure 15
Skin thickness of hairless mice after CAE treatment. Significant difference versus the normal group: ###, p < 0.001; significant difference versus the UVB-induced group: ***, p < 0.001.
Figure 16
Figure 16
Light micrographs of histological sections of hairless mice stained with Masson’s trichrome. Collagen fibers were stained blue. UVB exposure reduced the collagen content in the mouse skin dermis and CAE treatment restored the collagen content.
Figure 17
Figure 17
Immunohistological staining for MMP-1 in the hairless mouse skin after UVB exposure and CAE treatment. MMP-1 expression increased after UVB irradiation in the mouse skin, whereas CAE treatment inhibited the effect.
Figure 18
Figure 18
Immunohistological staining for iNOS in the hairless mouse skin after UVB exposure and CAE treatment.
Figure 19
Figure 19
Immunohistological staining for IL-6 in the hairless mouse skin after UVB exposure and CAE treatment.
Figure 20
Figure 20
Immunohistological staining for NF-κB in the hairless mouse skin after UVB exposure and CAE treatment.
Figure 21
Figure 21
Scheme of CAE inhibition of UVB-induced inflammation and photodamage. (↑: upregulation; ─┤inhibition; red circles: inhibition)
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