Ultraviolet B-induced Skin Damage Research Articles

Inhibiting Neutrophil Extracellular Traps Protects against Ultraviolet B-Induced Skin Damage: Effects of Hochu-ekki-to and DNase I.

UV-B radiation induces sunburn, and neutrophils are pivotal in this inflammation. In this study, we examined the potential involvement of neutrophil extracellular traps (NETs) in ultraviolet B (UVB)-induced skin inflammation, correlating the skin inflammation-mitigating effects of Hochu-ekki-to on UV-B irradiation and NETs. To elucidate NET distribution in the dorsal skin, male ICR mice, exposed to UVB irradiation, were immunohistologically analyzed to detect citrullinated histone H3 (citH3) and peptidylarginine deiminase 4 (PAD4). Reactive oxygen species (ROS) production in the bloodstream was analyzed. To establish the involvement of NET-released DNA in this inflammatory response, mice were UV-B irradiated following the intraperitoneal administration of DNase I. In vitro experiments were performed to scrutinize the impact of Hochu-ekki-to on A23187-induced NETs in neutrophil-like HL-60 cells. UV-B irradiation induced dorsal skin inflammation, coinciding with a significant increase in citH3 and PAD4 expression. Administration of DNase I attenuated UV-B-induced skin inflammation, whereas Hochu-ekki-to administration considerably suppressed the inflammation, correlating with diminished levels of citH3 and PAD4 in the dorsal skin. UV-B irradiation conspicuously augmented ROS and hydrogen peroxide (H2O2) production in the blood. Hochu-ekki-to significantly inhibited ROS and H2O2 generation. In vitro experiments demonstrated that Hochu-ekki-to notably inhibited A23187-induced NETs in differentiated neutrophil-like cells. Hence, NETs have been implicated in UV-B-induced skin inflammation, and their inhibition reduces cutaneous inflammation. Additionally, Hochu-ekki-to mitigated skin inflammation by impeding neutrophil infiltration and NETs in the dorsal skin of mice.

Prevention and Repair of Ultraviolet B-Induced Skin Damage in Hairless Mice via Transdermal Delivery of Growth Factors Immobilized in a Gel-in-Oil Nanoemulsion.

Ultraviolet (UV) radiation from the sun or artificial sources is one of the primary causes of skin damage, including sunburns, tanning, erythema, and skin cancer. Among the three different types of UV rays, UVB rays have a medium wavelength that can penetrate the epidermal layer of the skin, resulting in sunburn, suntan, blistering, and melanoma in case of chronic exposure. This study aimed to evaluate the preventive and therapeutic effects of a gel-in-oil nanogel dispersion (G/O-NGD) as a transdermal delivery biomolecular carrier for skin damage caused by UVB light. The efficacy of this carrier against UVB-induced skin damage was investigated in vivo by delivering different growth factors (GFs) encapsulated in a G/O-NGD. Artificial UVB light was used to induce skin damage in nude mice, followed by the transdermal application of five GF [vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), epidermal growth factor (EGF), transforming growth factor (TGF)-1, and insulin-like growth factor (IGF)-α]-immobilized G/O-NGD. Among these GFs, VEGF and bFGF promoted angiogenesis, while EGF, TGF-1, and IGF-α promoted the repair and regeneration of damaged cells. The results showed that G/O-NGD was superior to heparin-immobilized G/O-NGD in reducing UVB-induced skin damage, such as erythema, epidermal water reduction, inflammation, and dermis thickening. In addition, G/O-NGD could prevent and treat abnormal follicle proliferation caused by UVB rays and exhibited potential to repair lipid glands. Overall, our results demonstrate the potential of G/O-NGDs for the treatment of UVB-induced skin damage.

The Relationship Between Ultraviolet B and DNA Methylation in Skin Cancers

Ultraviolet B is regarded as an important factor in many skin diseases, especially skin cancers. Increasingly more evidence is showing that changes in DNA methylation occur in patients with skin cancers. Changes in DNA methylation have also been observed in ultraviolet B-irradiated cells and mouse models. DNA methylation modifier enzymes are simultaneously affected. We herein review the evidence to date showing that Ultraviolet B affects changes in DNA methylation modifier enzymes in skin cancers. However, the mechanism of how ultraviolet B regulates the changes in DNA methylation modifier enzymes remains to be further elucidated. Understanding the mechanism by which ultraviolet B modulates DNA methylation modifier enzymes can help to identify potential therapeutic markers or targets and develop novel strategies for preventing or treating ultraviolet B-induced skin damage.

Persimmon oligomeric proanthocyanidins alleviate ultraviolet B-induced skin damage by regulating oxidative stress and inflammatory responses

Skin damage can be induced by excessive ultraviolet B (UV-B) irradiation. This study aimed to investigate the potential protective activity of persimmon oligo-proanthocyanidins (P-OPC) against UV-B induced human keratinocyte cells (HaCaT cells) and skin damage and its underlying mechanisms in vitro and in vivo. P-OPC was shown to inhibit the production of intracellular reactive oxygen species (ROS) induced by UVB radiation in both HaCaT cells and mouse skin tissues by increasing the activity of the antioxidant enzyme system [superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and glutathione (GSH)]. Furthermore, P-OPC was found to suppress cell apoptosis and the production of inflammatory cytokines, TNF-α, and IL-6. Overall, P-OPC could protect skin tissues from UV-B-induced damage by suppressing oxidant stress, acute inflammation, and cell apoptosis via regulating MAPK and NF-κB signalling pathways. These results indicate the potential of P-OPC as a photochemo-protective agent against UV-B induced skin damage.

Potential Photoprotective Effect of Dietary Corn Silk Extract on Ultraviolet B-Induced Skin Damage.

Ultraviolet B (UVB) irradiation causes adverse effects on the skin. Corn silk contains flavonoids and other bioactive compounds and antioxidants, which may prevent skin photoaging through antioxidant and anti-inflammatory effects. We aimed to investigate the potential photoprotective effects of dietary corn silk on UVB-induced skin damage in mice and the mechanisms behind these effects on human skin cells. Oral administration of corn silk water extract (CS) (2 or 4 g/kg/day) for 19 weeks decreased epidermal thickness, wrinkle formation, and positive staining for PCNA, Ki67, and 8-OHdG, and increased collagen staining in UVB-irradiated SKH-1 hairless mice compared with controls. The pro-inflammatory NF-κB target genes (IL-1β, iNOS, and COX-2) and MMP-9 expressions were lower in the CS groups, and TGF-β/Smad signaling increased. Low skin lipid peroxidation and blood DNA oxidation levels and high blood glutathione were detected. Antioxidant transcription factor Nrf2-related catalase and SOD1 proteins and glutaredoxin mRNA levels increased. The results of CS extract treatment and UVB irradiation in HaCaT cells showed the same results in Nrf2 and NF-κB target genes. An LC-MS/MS analysis showed that the CS extract contained potential antioxidants, which might have contributed to its anti-photoaging effects in tissues and cells. CS extract may reduce UVB-induced skin damage through antioxidant and anti-inflammatory mechanisms.

Protective Effect of Sulfated Polysaccharides from Celluclast-Assisted Extract of Hizikia fusiforme Against Ultraviolet B-Induced Skin Damage by Regulating NF-κB, AP-1, and MAPKs Signaling Pathways In Vitro in Human Dermal Fibroblasts.

Our previous study evaluated the antioxidant activities of sulfated polysaccharides from Celluclast-assisted extract of Hizikia fusiforme (HFPS) in vitro in Vero cells and in vivo in zebrafish. The results showed that HFPS possesses strong antioxidant activity and suggested the potential photo-protective activities of HFPS. Hence, in the present study, we investigated the protective effects of HFPS against ultraviolet (UV) B-induced skin damage in vitro in human dermal fibroblasts (HDF cells). The results indicate that HFPS significantly reduced intracellular reactive oxygen species (ROS) level and improved the viability of UVB-irradiated HDF cells in a dose-dependent manner. Furthermore, HFPS significantly inhibited intracellular collagenase and elastase activities, remarkably protected collagen synthesis, and reduced matrix metalloproteinases (MMPs) expression by regulating nuclear factor kappa B (NF-κB), activator protein 1 (AP-1), and mitogen-activated protein kinases (MAPKs) signaling pathways in UVB-irradiated HDF cells. These results suggest that HFPS possesses strong UV protective effect, and can be a potential ingredient in the pharmaceutical and cosmetic industries.

Protective effect of (-)-epigallocatechin gallate on ultraviolet b-induced skin damage in hairless mice

Purpose : To investigate the protective effect of green tea (-)-epigallocatechin gallate (EGCg) on ultraviolet B (UV-B)-induced skin damages in hairless mice in order to develop a natural sunscreen compound for use in skin care products and cosmetics. Methods : EGCg was dissolved in acetone at concentrations of 1.0, 10.0 and 50.0 mg/mL, and topically applied to the skin of hairless mice at doses of 0.2 mL/cm2, with acetone as control. The mice were then irradiated by 100 μW/cm2 UV-B for 30 min daily. EGCg treatment and UV-B irradiation were carried out daily for 28 consecutive days. The mice were then sacrificed and their dorsal skin examined by transmission electron microscopy (TEM) on the 28th day. Results : UV-B irradiation induced severe macroscopic skin damage including chapping, cracking and abnormal desquamation in the treated hairless mice. EGCg showed dose-dependent protective effects against UV-B induced damage on the skin. Treatments with 10.0 and 50.0 mg/mL EGCg alleviated UVB- induced skin damage by suppressing both keratinocyte apoptosis and mitochondrial dysfunction, along with inhibiting the production of melanin pigment. Conclusion : Topical application of green tea EGCg shows dose-dependent protective effect against UV-B-induced damage on hairless mouse skin. Thus, the plant compound can potentially be used as an alternative agent for photoprotection against UV-B exposure. Keywords : UV-B, Green tea EGCg, Photoprotection, Stratum corneum, Mitochondrion, Melanosome

Naringin protects ultraviolet B-induced skin damage by regulating p38 MAPK signal pathway

BackgroundNaringin is a bioflavonoid and has free radical scavenging and anti-inflammatory properties. MethodsWe examined the effects of naringin on skin after ultraviolet radiation B (UVB) irradiation and the signal pathways by in vitro and in vivo assay. ResultsHaCaT cells pretreated with naringin significantly inhibited UVB induced-cell apoptosis and production of intracellular reactive oxygen species (ROS). The expressions of interleukin-1β (IL-1β), interleukin-6 (IL-6), interleukin-8 (IL-8) and cyclooxygenase-2 (COX-2) in HaCaT cells pretreated with naringin were decreased compared with the only UVB group. Also, the activation of p38 induced by UVB in HaCaT cells was reversed by naringin treatments. The inhibition function of naringin on p38 activity was more obvious than JNK. In vivo, topical treatments with naringin prevented the increase of epidermal thickness, IL-6 production, cell apoptosis and the overexpression of COX-2 in BALB/c mice skin irradiated with UVB. Naringin treatment also markedly blocked the activation of p38 in response to UVB stimulation in the mouse skin. ConclusionNaringin can effectively protect against UVB-induced keratinocyte apoptosis and skin damage by inhibiting ROS production, COX-2 overexpression and strong inflammation reactions. It seemed that naringin played its role against UVB-induced skin damage through inhibition of mitogen-activated protein kinase (MAPK)/p38 activation.

Evaluating the Effect of Algal Extracts against Ultraviolet B-Induced Skin Damage in BALB/c Mice

Ethanol extract of mixed algae—spirogyra and ulothrix was investigated to assess the effect on some biochemical parameters in UVB irradiated mice. The dorsal-thoracic region of mice were shaved and exposed to UVB radiation for 24 h for two consecutive weeks. Five groups of ten mice each were conducted: non-irradiated control and irradiated control. Mice treated with commercial cream (S.M.) at a dose of 0.1 mg/cm 2 and mice treated with ethanol extract of mixed spirogyra and ulothrix at a dose of 0.1 mg/cm 2 or 0.2 mg/cm 2 . Topical application was performed to all treated mice groups once a day for four consecutive weeks. Results showed significant differences between treated and control groups during the whole period of experiment. The clear potentiality of the ethanol extract was detected through body and skin weight, level of total protein, Superoxide Dismutase (SOD) and Catalase (CAT) activities in skin. However, UVB irradiated mice treated with 0.2 mg/cm 2 exhibited the most significant effect when compared to control groups. That may be attributed to anti-inflammatory and anti-oxidant effects of algal extract.

Effects of Porcine Placenta Extract Ingestion on Ultraviolet B-induced Skin Damage in Hairless Mice

The aim of our study was to evaluate the potential benefits of an oral supplement containing porcine placenta extract (PPE) on skin parameters related to cutaneous physiology and aging. PPEs were administered orally to hairless mice for 12 wk. The effects of oral PPE administration on skin water-holding capacity and Transepidermal Water Loss (TEWL) were similar to those of oral collagen (HYCPU2) administered as a positive control. Magnified photographs and replica images showed a reduction in UVB-induced wrinkle formation after collagen and PPE treatments. PPE treatments ameliorated the thicker skin surface that results from UVB exposure, based on a histological examination of skin tissue. The groups that were orally administered PPE (0.05%, OL; 0.1%, OH group) showed significantly reduced Matrix Metaloproteinase-2 (MMP-2) mRNA expression levels compared with the UVB control (Con), by 33.5% and 35.2%, respectively. The mRNA expression of another collagen-degrading protein, MMP-9, was also significantly lower in the groups that received oral administration of PPE (especially in the OH group) than in the control group. Additionally, oral administration of PPE significantly upregulated tissue inhibitor of metalloproteinase-1 (TIMP-1) and -2 mRNA expression levels compared with expression levels in the control group (p<0.05). This indicates that orally administered PPE activated the expression of Timp-1 and -2, inhibitors of MMP, which is responsible for collagen degradation in skin. Taken together, we propose that long-term oral administration of PPE might have a beneficial effect with respect to skin photo-aging.

Artocarpin attenuates ultraviolet B-induced skin damage in hairless mice by antioxidant and anti-inflammatory effects

Artocarpin attenuates ultraviolet B-induced skin damage in hairless mice by antioxidant and anti-inflammatory effects

Artocarpin attenuates ultraviolet B-induced skin damage in hairless mice by antioxidant and anti-inflammatory effect

Artocarpin, a prenylated flavonoid isolated from an agricultural plant Artocarpus communis, has been documented to possess anti-inflammation and anticancer activities. As oxidative stress and inflammation promote the development of ultraviolet B (UVB) irradiation-induced photodamage, the aim of the present study was to evaluate the photoprotective effect of artocarpin on UVB-induced skin damage in hairless mice. Artocarpin at a topical dose of 0.05% and 0.1% showed a significant photoprotective effect by decreasing histopathological changes, such as desquamation, epidermal thicken and sunburn cell formation, but 0.1% of artocarpin administration did not show better effect. Regarding the antioxidant activities, artocarpin exhibited a significant effect (P<0.05) by decreasing levels of reactive species oxygen and lipid peroxidation. In addition, artocarpin can significant decrease the level of tumor necrosis factor-α and interleukin-1β for downregulating the inflammation protein, including the synthesis of cytosolic phospholipase A2 and cyclooxygenase-2 (P<0.05). In conclusion, these data suggest that artocarpin can prevent skin damage from UVB irradiation-induced photodamage in hairless mice and this is likely mediated through its antioxidant and anti-inflammation mechanisms. Therefore, we suggested that artocarpin could be a useful photoprotective agent in medicine and/or cosmetics.

Protective effect of GSW against UVB‐induced skin damage

Ultraviolet B (UVB) irradiation on skin can induce the production of reactive oxygen species (ROS) which damage cellular components. Increased ROS in skin cause activation of the activator protein‐1 (AP‐1) transcription factor, which increases matrix metalloproteinases (MMPs) expression and collagen degradation. These causes the characteristic changes of photoaging induced by UVB irradiation. In this study, we investigated the protective effects of GSW against UVB induced skin damage in human skin fibroblasts. GSW was first analyzed for antioxidant activity using DPPH and ABTs radical scavenging assay. DPPH and ABTs radical scavenging activities of GSW were significantly higher in a dose‐dependent manner. Skin fibroblast were treated vitamin C and GSW (10μg/mL, 30μg/mL, 50μg/mL) after UVB irradiation (0mJ/cm2 and 25mJ/cm2). Vitamin C and GSW inhibited MMPs (MMP‐1, MMP‐3, MMP‐9) expression and MMP‐1 secretion caused by UVB irradiation. Moreover, we found that treatment with vitamin C and GSW significantly increased type‐1 collagen expression and production. We next examined the levels of antioxidative enzymes (SOD, Catalase, GPx) activities related in antioxidative effects. Reduced antioxidative enzymes activities by UVB irradiation were increased after treatment with vitamin C and GSW. In conclusion, theses results show that GSW has protective effects on UVB‐induced skin damage in human skin fibroblasts by regulating antioxidative defence systems and MMPs expression.

Protective Effect of α-Tocopherol-6-O-Phosphate Against Ultraviolet B-Induced Damage in Cultured Mouse Skin

The ability of the novel water-soluble provitamin E, alpha-tocopherol-6-O-phosphate, to protect against ultraviolet B-induced damage in cultured mouse skin was investigated and compared with the protectiveness of alpha-tocopherol acetate in cultured mouse skin. Pretreatment of skin with 0.5% (9.4 mM) alpha-tocopherol-6-O-phosphate in medium for 3 h significantly prevented such photodamage as sunburn cell formation, DNA degradation, and lipid peroxidation, which were induced in control cultured skin by a single dose of ultraviolet B irradiation at 0 to 40 kJ per m2 (290-380 nm, maximum 312 nm). This protection was greater than that seen with alpha-tocopherol acetate, the most common provitamin E that is used in commercial human skin care products. The concentration of alpha-tocopherol in cultured skin pretreated with 0.5% alpha-tocopherol-6-O-phosphate rose to approximately two to three times that found in the control skin and the reduction in cutaneous alpha-tocopherol that was induced by ultraviolet irradiation was significantly inhibited. In the group pretreated with 0.5% alpha-tocopherol acetate, however, conversion of alpha-tocopherol acetate to alpha-tocopherol was not observed, although the level of provitamin incorporated into the cultured skin was the same as that for alpha-tocopherol-6-O-phosphate. These findings indicated that the enhanced ability of alpha-tocopherol-6-O-phosphate to protect against ultraviolet B-induced skin damage compared with alpha-tocopherol acetate may have been due to alpha-tocopherol-6-O-phosphate's conversion to alpha-tocopherol. Moreover, following pretreatment with a 0.5% alpha-tocopherol-6-O-phosphate, alpha-tocopherol-6-O-phosphate was incorporated into the human skin in a three-dimensional model and 5% of the incorporated alpha-tocopherol-6-O-phosphate was converted to alpha-tocopherol. These results suggest that treatment with the novel provitamin E, alpha-tocopherol-6-O-phosphate may be useful in preventing ultraviolet-induced human skin damage.