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Prevention of UV-induced skin damages by 11,14,17-eicosatrienoic acid in hairless mice in vivo.

Jin XJ, Kim EJ, Oh IK, Kim YK, Park CH, Chung JH - J. Korean Med. Sci. (2010)

Bottom Line: Recent studies have shown that some omega-3 (omega-3) PUFAs, such as eicosapentaenoic acid (EPA) and dodecahexaenoic acid (DHA), have protective effects on acute and chronic UV-induced changes.However, the effects of other omega-3 PUFAs including 11,14,17-eicosatrienoic acid (20:3) (ETA) on UV-induced skin damages are poorly understood.We found that topical treatment with ETA attenuated UV-induced epidermal and dermal thickness and infiltration of inflammatory cells, and impairment of skin barrier function.

View Article: PubMed Central - PubMed

Affiliation: Department of Dermatology, Seoul Nationa University College of Medicine, Seoul, Korea.

ABSTRACT
Polyunsaturated fatty acids (PUFAs) are known to play important roles in various physiological and pathological processes. Recent studies have shown that some omega-3 (omega-3) PUFAs, such as eicosapentaenoic acid (EPA) and dodecahexaenoic acid (DHA), have protective effects on acute and chronic UV-induced changes. However, the effects of other omega-3 PUFAs including 11,14,17-eicosatrienoic acid (20:3) (ETA) on UV-induced skin damages are poorly understood. In this study, we investigated the cutaneous photoprotective effects of ETA in hairless mice in vivo. Female HR-1 hairless mice were topically treated with vehicle (ethanol:polyethylene glycol=30:70) only, 0.1% ETA, or 1% ETA once a day for 3 successive days after one time UV irradiation (200 mJ/cm(2)) on dorsal skins. Skin biopsy was carried out on the fourth day (72 hr after UV irradiation). We found that topical treatment with ETA attenuated UV-induced epidermal and dermal thickness and infiltration of inflammatory cells, and impairment of skin barrier function. In addition, ETA suppressed the expression of IL-1beta, COX-2, and MMP-13 induced by UV irradiation. Our results show that the topical application of ETA protects against UV-induced skin damage in hairless mice and suggest that ETA can be a potential agent for preventing and/or treating UV-induced inflammation and photoaging.

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ETA increases IκBα expression and decreases NF-κB p65 phosphorylation in hairless mouse skin in vivo. Female HR-1 hairless mice were topically treated with vehicle (ethanol : polyethylene glycol=30:70) only, 0.1% ETA or 1% ETA once a day for 3 successive days after one time irradiation of UV (200 mJ/cm2) on dorsal skins. Skin biopsy was carried out on the fourth day (72 h after UV irradiation). (A) Expression of IκBα was detected by western blot analysis. (B) Phospho-NF-κB p65 was detected by western blot analysis. Results are expressed as fold change. Values are mean±SEM (n=8).*P<0.001 vs. control (CON) vehicle group; †P<0.05, ‡P<0.001 vs. UV-irradiated (UV) vehicle group.
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Figure 5: ETA increases IκBα expression and decreases NF-κB p65 phosphorylation in hairless mouse skin in vivo. Female HR-1 hairless mice were topically treated with vehicle (ethanol : polyethylene glycol=30:70) only, 0.1% ETA or 1% ETA once a day for 3 successive days after one time irradiation of UV (200 mJ/cm2) on dorsal skins. Skin biopsy was carried out on the fourth day (72 h after UV irradiation). (A) Expression of IκBα was detected by western blot analysis. (B) Phospho-NF-κB p65 was detected by western blot analysis. Results are expressed as fold change. Values are mean±SEM (n=8).*P<0.001 vs. control (CON) vehicle group; †P<0.05, ‡P<0.001 vs. UV-irradiated (UV) vehicle group.

Mentions: It has been reported that the transcription factor nuclear factor-κB (NF-κB) plays an important role on expression of IL-1β and COX-2 induced by various stimuli (24). In unstimulated cells, NF-κB is present in the cytoplasm as complexes with one of three isoforms (α, β, or ε) of inhibitor of κB (IκB). Upon stimulation with extracellular stimuli including proinflammatory cytokines or UV, the inhibitor of κB kinase (IKK) phosphorylates IκB proteins, targeting them for proteolysis, which leads to translocation of NF-κB into the nucleus where NF-κB induces transcriptional activation of a variety of genes, including proinflammatory cytokines, chemokines, COX-2, and MMPs (25). In addition, NF-κB activity has been shown to be regulated by the phosphorylation of NF-κB p65 (26, 27). To study how ETA affects the molecular events involved in the regulation of NF-κB activity by UV in hairless mice in vivo, we investigated the effects of ETA on UV-induced regulation of IκBα expression and NF-κB p65 phosphorylation. Topical treatment of ETA increased IκBα protein levels in both control group and UV-irradiated group (Fig. 5A). Basal levels of phospho-NF-κB p65 were not affected by ETA but UV-induced levels of phospho-NF-κB p65 were decreased dose-dependently by treatment with ETA (Fig. 5B), indicating that ETA can attenuate UV-induced NF-κB activation. These results suggest that ETA may inhibit UV-induced expression of IL-1β, COX-2 and MMP-13 through the regulation of NF-κB signaling pathways.


Prevention of UV-induced skin damages by 11,14,17-eicosatrienoic acid in hairless mice in vivo.

Jin XJ, Kim EJ, Oh IK, Kim YK, Park CH, Chung JH - J. Korean Med. Sci. (2010)

ETA increases IκBα expression and decreases NF-κB p65 phosphorylation in hairless mouse skin in vivo. Female HR-1 hairless mice were topically treated with vehicle (ethanol : polyethylene glycol=30:70) only, 0.1% ETA or 1% ETA once a day for 3 successive days after one time irradiation of UV (200 mJ/cm2) on dorsal skins. Skin biopsy was carried out on the fourth day (72 h after UV irradiation). (A) Expression of IκBα was detected by western blot analysis. (B) Phospho-NF-κB p65 was detected by western blot analysis. Results are expressed as fold change. Values are mean±SEM (n=8).*P<0.001 vs. control (CON) vehicle group; †P<0.05, ‡P<0.001 vs. UV-irradiated (UV) vehicle group.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2877234&req=5

Figure 5: ETA increases IκBα expression and decreases NF-κB p65 phosphorylation in hairless mouse skin in vivo. Female HR-1 hairless mice were topically treated with vehicle (ethanol : polyethylene glycol=30:70) only, 0.1% ETA or 1% ETA once a day for 3 successive days after one time irradiation of UV (200 mJ/cm2) on dorsal skins. Skin biopsy was carried out on the fourth day (72 h after UV irradiation). (A) Expression of IκBα was detected by western blot analysis. (B) Phospho-NF-κB p65 was detected by western blot analysis. Results are expressed as fold change. Values are mean±SEM (n=8).*P<0.001 vs. control (CON) vehicle group; †P<0.05, ‡P<0.001 vs. UV-irradiated (UV) vehicle group.
Mentions: It has been reported that the transcription factor nuclear factor-κB (NF-κB) plays an important role on expression of IL-1β and COX-2 induced by various stimuli (24). In unstimulated cells, NF-κB is present in the cytoplasm as complexes with one of three isoforms (α, β, or ε) of inhibitor of κB (IκB). Upon stimulation with extracellular stimuli including proinflammatory cytokines or UV, the inhibitor of κB kinase (IKK) phosphorylates IκB proteins, targeting them for proteolysis, which leads to translocation of NF-κB into the nucleus where NF-κB induces transcriptional activation of a variety of genes, including proinflammatory cytokines, chemokines, COX-2, and MMPs (25). In addition, NF-κB activity has been shown to be regulated by the phosphorylation of NF-κB p65 (26, 27). To study how ETA affects the molecular events involved in the regulation of NF-κB activity by UV in hairless mice in vivo, we investigated the effects of ETA on UV-induced regulation of IκBα expression and NF-κB p65 phosphorylation. Topical treatment of ETA increased IκBα protein levels in both control group and UV-irradiated group (Fig. 5A). Basal levels of phospho-NF-κB p65 were not affected by ETA but UV-induced levels of phospho-NF-κB p65 were decreased dose-dependently by treatment with ETA (Fig. 5B), indicating that ETA can attenuate UV-induced NF-κB activation. These results suggest that ETA may inhibit UV-induced expression of IL-1β, COX-2 and MMP-13 through the regulation of NF-κB signaling pathways.

Bottom Line: Recent studies have shown that some omega-3 (omega-3) PUFAs, such as eicosapentaenoic acid (EPA) and dodecahexaenoic acid (DHA), have protective effects on acute and chronic UV-induced changes.However, the effects of other omega-3 PUFAs including 11,14,17-eicosatrienoic acid (20:3) (ETA) on UV-induced skin damages are poorly understood.We found that topical treatment with ETA attenuated UV-induced epidermal and dermal thickness and infiltration of inflammatory cells, and impairment of skin barrier function.

View Article: PubMed Central - PubMed

Affiliation: Department of Dermatology, Seoul Nationa University College of Medicine, Seoul, Korea.

ABSTRACT
Polyunsaturated fatty acids (PUFAs) are known to play important roles in various physiological and pathological processes. Recent studies have shown that some omega-3 (omega-3) PUFAs, such as eicosapentaenoic acid (EPA) and dodecahexaenoic acid (DHA), have protective effects on acute and chronic UV-induced changes. However, the effects of other omega-3 PUFAs including 11,14,17-eicosatrienoic acid (20:3) (ETA) on UV-induced skin damages are poorly understood. In this study, we investigated the cutaneous photoprotective effects of ETA in hairless mice in vivo. Female HR-1 hairless mice were topically treated with vehicle (ethanol:polyethylene glycol=30:70) only, 0.1% ETA, or 1% ETA once a day for 3 successive days after one time UV irradiation (200 mJ/cm(2)) on dorsal skins. Skin biopsy was carried out on the fourth day (72 hr after UV irradiation). We found that topical treatment with ETA attenuated UV-induced epidermal and dermal thickness and infiltration of inflammatory cells, and impairment of skin barrier function. In addition, ETA suppressed the expression of IL-1beta, COX-2, and MMP-13 induced by UV irradiation. Our results show that the topical application of ETA protects against UV-induced skin damage in hairless mice and suggest that ETA can be a potential agent for preventing and/or treating UV-induced inflammation and photoaging.

Show MeSH
Related in: MedlinePlus