147 UVB irradiation induces barrier dysfunction in epidermal keratinocytes, which can be repaired by ethanol extract of peanut sprouts, a new antioxidant to be originated from peanuts

Once weak ultraviolet ray-B (UVB) irradiates the skin cells, the generation of reactive nitrogen species (RNS), but not reactive oxygen species (ROS), is stimulated for the mislocalization of claudin-1 (CLDN1), an essential protein for forming tight junctions (TJs). Since our skin is constantly exposed to sunlight throughout our lives, an effective protection strategy is needed to maintain the skin barrier against weak UVB. In the present study, we investigated whether an ethanol extract of Brazilian green propolis (EBGP) and flavonoids had a protective effect against weak UVB irradiation-induced barrier dysfunction in human keratinocyte-derived HaCaT cells. A pretreatment with EBGP suppressed TJ permeability, RNS production, and the nitration level of CLDN1 in the weak UVB-exposed cells. Among the propolis components, apigenin and apigenin-like flavonoids have potent protective effects against NO production and the mislocalization of CLDN1 induced by UVB. The analyses between structures and biological function revealed that the chemically and structurally characteristic flavonoids with a hydroxyl group at the 4′ position on the B-ring might contribute to its protective effect on barrier dysfunction caused by weak UVB irradiation. In conclusion, EBGP and its component apigenin protect HaCaT cells from weak UVB irradiation-induced TJ barrier dysfunction mediated by suppressing NO production.

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Sargassum fulvellumProtects HaCaT Cells and BALB/c Mice from UVB-Induced Proinflammatory Responses

Evidence-based Complementary and Alternative Medicine ◽

10.1155/2013/747846 ◽

2013 ◽

Vol 2013 ◽

pp. 1-10 ◽

Cited By ~ 4

Author(s):

Chan Lee ◽

Gyu Hwan Park ◽

Eun Mi Ahn ◽

Chan-Ik Park ◽

Jung-Hee Jang

Keyword(s):

Nitric Oxide ◽

Ethanol Extract ◽

Prostaglandin E ◽

Hacat Cells ◽

Uvb Irradiation ◽

Proinflammatory Mediators ◽

Sargassum Fulvellum ◽

Cox 2 ◽

Anti Inflammatory ◽

Skin Damages

Ultraviolet (UV) radiation has been reported to induce cutaneous inflammation such as erythema and edema via induction of proinflammatory enzymes and mediators.Sargassum fulvellumis a brown alga of Sargassaceae family which has been demonstrated to exhibit antipyretic, analgesic, antiedema, antioxidant, antitumor, fibrinolytic, and hepatoprotective activities. The purpose of this study is to investigate anti-inflammatory effects of ethylacetate fraction of ethanol extract ofSargassum fulvellum(SFE-EtOAc) in HaCaT keratinocytes and BALB/c mice. In HaCaT cells, SFE-EtOAc effectively inhibited UVB-induced cytotoxicity (60 mJ/cm2) and the expression of proinflammatory proteins such as cyclooxygenase-2 (COX-2), tumor necrosis factor-α(TNF-α), and inducible nitric oxide synthase (iNOS). Furthermore, SFE-EtOAc significantly reduced UVB-induced production of proinflammatory mediators including prostaglandin E2(PGE2) and nitric oxide (NO). In BALB/c mice, topical application of SFE-EtOAc prior to UVB irradiation (200 mJ/cm2) effectively suppressed the UVB-induced protein expression of COX-2, iNOS, and TNF-αand subsequently attenuated generation of PGE2and NO as well. In another experiment, SFE-EtOAc pretreatment suppressed UVB-induced reactive oxygen species production and exhibited an antioxidant potential by upregulation of antioxidant enzymes such as catalase and Cu/Zn-superoxide dismutase in HaCaT cells. These results suggest that SFE-EtOAc could be an effective anti-inflammatory agent protecting against UVB irradiation-induced skin damages.

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Up-regulation of hyaluronan synthase genes in cultured human epidermal keratinocytes by UVB irradiation

Archives of Biochemistry and Biophysics ◽

10.1016/j.abb.2007.12.004 ◽

2008 ◽

Vol 471 (1) ◽

pp. 85-93 ◽

Cited By ~ 21

Author(s):

Ikuko Kakizaki ◽

Naoki Itano ◽

Koji Kimata ◽

Katsumi Hanada ◽

Atsushi Kon ◽

...

Keyword(s):

Hyaluronan Synthase ◽

Epidermal Keratinocytes ◽

Human Epidermal Keratinocytes ◽

Uvb Irradiation

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Transcriptional Activation of Endogenous Retroviral Sequences in Human Epidermal Keratinocytes by UVB Irradiation

Journal of Investigative Dermatology ◽

10.1046/j.1523-1747.1999.00728.x ◽

1999 ◽

Vol 113 (4) ◽

pp. 587-594 ◽

Cited By ~ 53

Author(s):

Christine Hohenadl ◽

Herbert Germaier ◽

Monika Walchner ◽

Manuela Hagenhofer ◽

Martin Herrmann ◽

...

Keyword(s):

Transcriptional Activation ◽

Epidermal Keratinocytes ◽

Human Epidermal Keratinocytes ◽

Uvb Irradiation

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Vascular endothelial growth factor promotes sensitivity to ultraviolet B–induced cutaneous photodamage

Blood ◽

10.1182/blood-2004-06-2435 ◽

2005 ◽

Vol 105 (6) ◽

pp. 2392-2399 ◽

Cited By ~ 47

Author(s):

Satoshi Hirakawa ◽

Seishiro Fujii ◽

Kentaro Kajiya ◽

Kiichiro Yano ◽

Michael Detmar

Keyword(s):

Vascular Endothelial Growth Factor ◽

Growth Factor ◽

Transgenic Mice ◽

Ultraviolet B ◽

Epidermal Keratinocytes ◽

Vascular Endothelial ◽

Wild Type ◽

Uvb Irradiation ◽

Uvb Exposure ◽

Endothelial Growth Factor

AbstractAcute ultraviolet B (UVB) irradiation of the skin results in erythema, vasodilation, edema, and angiogenesis, which is associated with the expression of vascular endothelial growth factor (VEGF) by epidermal keratinocytes. It is unclear, however, whether VEGF is required for the damage or repair process that occurs in the skin on UVB exposure. We subjected transgenic mice that overexpress VEGF, and their wild-type littermates, to graded doses of acute UVB irradiation. The skin of VEGF-overexpressing mice was highly photosensitive and became erythematic when exposed to half the UVB dose required to induce erythema in wild-type mice. Erythema was associated with proliferating dermal endothelial cells, cutaneous edema, and inflammatory cell infiltration. When subjected to 10 weeks of low-level UVB irradiation, no major changes were observed in wild-type mice, whereas VEGF transgenic mice developed skin damage associated with degradation of the dermal matrix and enhanced vascularization. Systemic treatment with an anti–VEGF blocking antibody reduced the sensitivity of wild-type mice to acute UVB irradiation without inhibiting post-UVB repair. Our results reveal that VEGF promotes the cutaneous damage that occurs after UVB exposure and that the VEGF signaling pathway might serve as a novel target for the prevention of UVB-induced photodamage.

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IL-24 Negatively Regulates Keratinocyte Differentiation Induced by Tapinarof, an Aryl Hydrocarbon Receptor Modulator: Implication in the Treatment of Atopic Dermatitis

International Journal of Molecular Sciences ◽

10.3390/ijms21249412 ◽

2020 ◽

Vol 21 (24) ◽

pp. 9412

Author(s):

Yen Hai Vu ◽

Akiko Hashimoto-Hachiya ◽

Masaki Takemura ◽

Ayako Yumine ◽

Yasutaka Mitamura ◽

...

Keyword(s):

Atopic Dermatitis ◽

Aryl Hydrocarbon Receptor ◽

Skin Barrier ◽

Janus Kinase ◽

Keratinocyte Differentiation ◽

Epidermal Keratinocytes ◽

Dependent Manner ◽

Jak Inhibitors ◽

Barrier Dysfunction ◽

Aryl Hydrocarbon

Skin barrier dysfunction, including reduced filaggrin (FLG) and loricrin (LOR) expression, plays a critical role in atopic dermatitis (AD) development. Since aryl hydrocarbon receptor (AHR), a ligand-activated transcription factor, mediates keratinocyte differentiation, it is a potential target for AD treatment. Recently, clinical studies have shown that tapinarof, an AHR modulator, attenuated the development of AD. To examine the molecular mechanism involved in this, we analyzed tapinarof-treated normal human epidermal keratinocytes (NHEKs). Tapinarof upregulated FLG and LOR mRNA and protein expression in an AHR-dependent manner. Tapinarof also induced the secretion of IL-24, a cytokine that activates Janus kinase (JAK)-signal transducer and activator of transcription (STAT), leading to the downregulation of FLG and LOR expression. Knockdown of either IL-24 or STAT3 expression by small interfering RNA (siRNA) transfection augmented the upregulation of FLG and LOR expression induced by tapinarof, suggesting that inhibition of the IL-24/STAT3 axis during AHR activation supports the improvement of skin barrier dysfunction. Furthermore, tapinarof alone could restore the downregulation of FLG and LOR expression induced by IL-4, a key cytokine of AD, and its combination with JAK inhibitors enhanced this effect. These findings provide a new strategy for treating AD using AHR modulators and JAK inhibitors.

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Acer palmatum thumb. Ethanol Extract Alleviates Interleukin-6-Induced Barrier Dysfunction and Dextran Sodium Sulfate-Induced Colitis by Improving Intestinal Barrier Function and Reducing Inflammation

Journal of Immunology Research ◽

10.1155/2018/5718396 ◽

2018 ◽

Vol 2018 ◽

pp. 1-10 ◽

Cited By ~ 6

Author(s):

Kwang-Youn Kim ◽

Tae-Woo Oh ◽

Hyun Ju Do ◽

Ju-Hye Yang ◽

In Jun Yang ◽

...

Keyword(s):

Interleukin 6 ◽

Barrier Function ◽

Sodium Sulfate ◽

Intestinal Barrier ◽

Ethanol Extract ◽

Dextran Sodium Sulfate ◽

Intestinal Barrier Function ◽

Control Group ◽

Barrier Dysfunction ◽

Acute Colitis

Ulcerative colitis is one inflammatory bowel disease (IBD) and is caused by diverse factors, including the extent and duration of intestinal inflammation. We investigated the effect of Acer palmatum thumb. ethanol extract (KIOM-2015E) on the expression of tight junction proteins and the levels of inflammation in the cell model induced with interleukin-6- (IL-6-) and mouse model of dextran sodium sulfate (DSS) induced with acute colitis. KIOM-2015E (100 mg/kg) was orally administered once per day to BALB/C mice with colitis induced by administration of 5% DSS in drinking water. KIOM-2015E did not affect viability in Caco-2 cells. Also, KIOM-2015E repaired the IL-6-induced intestinal barrier dysfunction in Caco-2 cells. Furthermore, KIOM-2015E recovered the loss of body weight and the abnormally short colon lengths in the DSS-induced model of acute colitis. Moreover, KIOM-2015E significantly inhibited the decrease of zonula occluden-1 and occludin in colonic tissue relative to the DSS-treated control group. KIOM-2015E also significantly inhibited the expression of IL-6 and tumor necrosis factor-α in the level of serum relative to the control group. Collectively, these data suggest that KIOM-2015E protects colitis principally by improving intestinal barrier function and promoting anti-inflammatory responses. In turn, these effects inhibit macrophage infiltration into the colon and thus may be a candidate treatment for IBD.

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Antiphotoaging and Antimelanogenic Effects of Penthorum chinense Pursh Ethanol Extract due to Antioxidant- and Autophagy-Inducing Properties

Oxidative Medicine and Cellular Longevity ◽

10.1155/2019/9679731 ◽

2019 ◽

Vol 2019 ◽

pp. 1-14 ◽

Cited By ~ 7

Author(s):

Deok Jeong ◽

Jongsung Lee ◽

Sang Hee Park ◽

You Ah Kim ◽

Byoung Jun Park ◽

...

Keyword(s):

Oxidative Stress ◽

Ethanol Extract ◽

Infectious Hepatitis ◽

Uvb Irradiation ◽

Protein Levels ◽

B16f10 Cells ◽

Penthorum Chinense Pursh ◽

Cox 2 ◽

Penthorum Chinense ◽

Melanin Contents

Ethnopharmacological Relevance. Penthorum chinense Pursh (Penthoraceae) is a traditional herbal plant that has been used in China for the treatment of jaundice, cholecystitis, edema, and infectious hepatitis. In addition, the Korea Medicinal Plant Dictionary states that Penthorum chinense Pursh can be used to treat contusions and skin bruises by improving blood flow. Recent studies have shown that Penthorum chinense Pursh ethanol extract (Pc-EE) exhibits strong antioxidant effects. In this study, we examined the effects of Pc-EE on UVB-induced or H2O2-induced oxidative stress, as well as its antimelanogenic properties. Cell viability, matrix metalloproteinase (MMP) expression, cyclooxygenease-2 (COX-2), and interleukin-6 (IL-6) expression and moisturizing factors were investigated in keratinocytes. Collagen synthesis induction was measured in HEK293T cells. For melanogenesis, the effects of Pc-EE on melanin content and tyrosinase activity were measured. Additionally, the antimelanogenic- and autophagy-inducing activities of Pc-EE were examined using immunoblotting and confocal microscopy. Pc-EE protected HaCaT cells against death from UVB irradiation- or H2O2-induced oxidative stress. Pc-EE increased the promoter activity of the type 1 procollagen gene Col1A1 and decreased the expression of MMPs, COX-2, IL-6, and hyaluronidase induced by UVB irradiation- or H2O2-induced oxidative stress. Pc-EE showed a strong antioxidant effect in the DPPH assay. In α-melanocyte-stimulating hormone- (α-MSH-) stimulated B16F10 cells, Pc-EE reduced melanin production, decreased tyrosinase expression and microphthalmia-associated transcription factor (MITF) protein levels, and decreased the phosphorylation levels of p38 and JNK. In HEK293T cells, Pc-EE promoted the expression of GFP-LC3B. In B16F10 cells, the LC3B and melanin contents were reduced by Pc-EE and were restored by the autophagy inhibitor 3-methyladenine (3-MA). These results suggest that Pc-EE can be used as a skin protection agent due to its antiapoptotic, antiaging, anti-inflammatory, and antimelanogenic properties.

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122 Epidermal keratinocytes express IL-13 mRNA and its expression induced by UVB irradiation precedes that of IL-10 mRNA

Journal of Dermatological Science ◽

10.1016/s0923-1811(97)81827-0 ◽

1997 ◽

Vol 15 (2) ◽

pp. 123

Author(s):

K. Katagiri ◽

S. Itami ◽

Y. Hatano ◽

H. Terashi ◽

S. Kurata ◽

...

Keyword(s):

Epidermal Keratinocytes ◽

Uvb Irradiation

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