UVA Exposure Research Articles

Assessment of the skin photoprotective capacities from coastal plant of Melaleuca cajuputi essential oil as a potential UV filters

UV irradiation can cause cutaneous damage that may be specific according to the wavelength of UV rays. For example, damage from UVB irradiation manifests itself in the form of sunburn cells and enhancement of the expression of p53, while damage from UVA exposure results in an increase in the expression of vimentin. These reactions to UV irradiation were used in this work to evaluate the photoprotective capacities of two sunblock preparations that were applied to the surface of the skin. One sunblock preparation is a UVB absorber containing the coastal plant of Melaleuca cajuputi essential oil and titanium oxide (TiO2) exclusively. The other sunblock preparation is a conventional sunblock containing oxybenzone as comparison. Result obtained for UV-Vis test was observed that the new formulation derived showed good absorption and exhibit high potential to be further develop as sunscreen in cosmeceutical applications

Protective effects of Thai silk sericins and their related mechanisms on UVA-induced phototoxicity and melanogenesis: Investigation in primary melanocyte cells using a proteomic approach

UV radiation causes excess production of melanin as a result of hyperpigmentation and skin disorders. Silk sericin exhibited bioactivities to skin and inhibited UV-induced phototoxicity and melanogenesis in skin cells; however, the mechanism related to sericin against UV-induced melanogenesis has not been investigated. This study aimed to investigate the protective effects of Thai silk sericins against UVA-induced phototoxicity and melanogenesis and their related mechanisms. Thai silk sericins exhibited cytoprotective effects against UV-induced toxicity in human primary melanocytes by attenuation of cytotoxicity, intracellular ROS generation, and mitochondrial potential impairment. Pre- and post-treatment with sericin significantly inhibited melanin synthesis and tyrosinase activity against UVA exposure. In addition, sericin S2 could reduce the basal melanin content in zebrafish embryos. The proteomic analysis demonstrated that Thai silk sericins altered the protein expression in melanocytes especially proteins related to stress, inflammatory, cytokine stimulation, cell proliferation, and cell survival processes that contribute to cytoprotective effect and inhibitory effect on melanogenesis of sericin. Moreover, we demonstrated the novel mechanism of Thai silk sericins in inhibiting UVA-induced melanogenesis via increasing BMP4 expression in MAPK/ERK signaling pathway. These evidences support the potential use of Thai silk sericins in prevention of hyperpigmentation in skin disorders especially after UVA exposure.

Deleterious impact of short duration UV-A exposure on the human sperm cell –An in vitro study

BackgroundEnvironmental stressors like radiation are a cause for male infertility. The quantum of UV-A in solar ultraviolet (UV) radiation surpasses the amount of UVB by 10 to 100 times, penetrates deeper than UV-B into tissue and mediates possible molecular damage, which warrants evaluation of the impact of UV-A on human spermatozoa. AimTo determine the differences in effects and responses of UV-A exposure on sperm cells from fertile volunteers and infertile men. Materials and MethodsThe study subjects were divided into Group I (Control) and Group II (Infertile). The impact of UV-A on sperm viability, nuclear integrity, chromatin maturity and DNA fragmentation (pre-and post-exposure) was evaluated using standard techniques. Antioxidant enzyme activity assays viz. Lipid Peroxidation (LPO), Superoxide Dismutase (SOD) and Catalase were also analysed. Statistical significance was considered at p < 0.05. ResultsThis study revealed significant decline in%viability in Group II after UV-A exposure when compared with pre-exposed Group I. The percent sperm with disrupted nuclear toroidal assembly significantly increased in infertile group after exposure, leaving the DNA vulnerable to damage. A significant elevation was observed in the percent immature forms correlated with the significant reduction in% halo formation (impaired nuclear chromatin decondensation) in both post-treated groups as compared to pre-treated groups, suggesting that disruption of sperm toroid triggers DNA damage. UV-A exposure resulted in increased LPO with decrease in antioxidant enzymes in these groups. The percent decline in viability, chromatin decondensation (halo) and antioxidant enzymes were higher in Group II than in Group I. In addition, the percent increase in disrupted toroids and immature chromatin in Group II suggested that the deleterious impact of UV-A on spermatozoa from the infertile group is significantly greater than that of fertile individuals. ConclusionThis study thus revealed that short term UV-A exposure adversely impacts spermatozoa of infertile males to a greater extent than that of the fertile group. Thus, specific awareness and precautions are imperative for occupationally exposed individuals.

Photo-aging evaluation - In vitro biological endpoints combined with collagen density assessment with multi-photon microscopy

BackgroundUltraviolet exposure has profound effect on the dermal connective tissue of human skin. ObjectiveWe aimed to develop and validate an evaluation method/methodology using a full-thickness reconstructed skin model, to assess the anti-photoaging efficacy of cosmetic ingredients and sunscreen formulas by blending multi relevant biological endpoints including the newly developed dermal collagen quantification method with Multi-photon microscopy. MethodsThe response of ex vivo human skin to UVA exposure was first characterized with multiphoton microscopy. Reconstructed full-thickness skin models was then used to reproduce the data and to create a proof-of-concept study by treating the models with sunscreen prototypes A or B, which differ on their UVA absorption properties, and systemic Vitamin C (Vit C). After exposure to UVA, the collagen density was quantified via multiphoton microscopy with automatic imaging processing. Histology, fibroblasts number, metalloprotease 1 (MMP1) secretion were also assessed. ResultsUVA exposure induced pronounced reduction in collagen density and increased MMP1 secretion within both ex vivo human skin and reconstructed skin. Histological damage and fibroblast disappearance was observed with reconstructed skin. Within the proof-of-concept study prototype B, possessing higher UVA filtration, gave better protection than prototype A on the UV associated biological markers, and association with Vit C boosted sunscreen formula efficacy. ConclusionsThe photoaging evaluation method, consists of multi biological markers as well as dermal collagen quantification, is a relevant mean to assess the pre-clinical efficacy of anti-photoaging ingredients and sunscreen products. This approach is also beneficial for evaluating the efficacy of sunscreens and photoprotective ingredients.

Formation of Cyclobutane Pyrimidine Dimers after UVA Exposure (Dark-CPDs) Is Inhibited by an Hydrophilic Extract of Polypodium leucotomos.

Exposure to sun and especially to ultraviolet radiation (UVR) exerts well known detrimental effects on skin which are implicated in malignancy. UVR induces production of cyclobutane pyrimidine dimers (CPDs), immediately during exposure and even hours after the exposure, these latter being called dark-CPDs, as consequence of the effects of different reactive species that are formed. Fernblock® (FB), an aqueous extract of Polypodium leucotomos, has proven to have photoprotective and antioxidant effects on skin. The aim of our work was to investigate the potential photoprotective effect of FB against dark-CPD formation. Murine melanocytes (B16-F10) were exposed to UVA radiation and the production of dark-CPDs and different reactive oxygen and nitrogen species (ROS and RNS) was measured. Significant dark-CPD formation could be seen at 3 h after UVA irradiation, which was inhibited by the pre-treatment of cells with FB. Formation of nitric oxide, superoxide and peroxynitrite was increased after irradiation, consistent with the increased CPD formation. FB successfully reduced the production of these reactive species. Hence, these results show how dark-CPDs are formed in UVA irradiated melanocytes, and that FB acts as a potential antioxidant and ROS scavenger, preventing the DNA damage induced by sun exposure.

Autophagy induction regulates aquaporin 3‐mediated skin fibroblast ageing*

Long- and short-term ultraviolet (UV) exposure have distinct biological effects on human fibroblasts. To elucidate the underlying mechanisms of the biological effects of UV exposure on human skin fibroblasts. We subjected human skin fibroblast cells with or without aquaporin 3 (AQP3), death effector domain-containing protein (DEDD) or Beclin1 manipulation to UVA treatment and evaluated autophagy and senescence in them. Short-term UVA irradiation induced autophagy and upregulated AQP3 but not senescence, whereas long-term UVA irradiation inhibited autophagy, AQP3 and trigger senescence in vitro and in vivo. Silencing AQP3 abolished short-term UVA irradiation-induced autophagy and led to cellular senescence, whereas AQP3 overexpression partially rescued the senescence and autophagy inhibition induced by long-term UVA exposure in vitro. Mechanistically, the transcription factor Jun was found to bind to the AQP3 promoter to activate its transcription following short-term UVA exposure. Subsequently, AQP3 interacted with DEDD to induce its ubiquitination-mediated degradation and promote autophagy, and bound to Beclin1 to directly activate autophagy. Finally, autophagy induced by AQP3 overexpression robustly prevented UVA-induced senescence in vitro and in vivo. Our study indicates that AQP3 controls skin fibroblast photoageing by regulating autophagy and represents a potential target for future interventions against skin ageing.

The photoprotective properties of \u03b1-tocopherol phosphate against long-wave UVA1 (385\xa0nm) radiation in keratinocytes in vitro

UVA1 radiation (340–400 nm), especially longwave UVA1 (> 370 nm), is often ignored when assessing sun protection due to its low sunburning potential, but it generates reactive oxygen species (ROS) and is poorly attenuated by sunscreens. This study aimed to investigate if α-tocopherol phosphate, (α-TP) a promising new antioxidant, could protect against long-wave UVA1 induced cell death and scavenge UVA1 induced ROS in a skin cell model. HaCaT keratinocyte cell viability (24 h) was assessed with Alamar Blue and Neutral Red assays. The metabolism of α-TP into α-T, assessed using mass spectrometry, and the compound's radical scavenging efficacy, assessed by the dichlorodihydrofluorescein (H2DCFDA) ROS detection assay, was monitored in HaCaTs. The mechanism of α-TP ROS scavenging was determined using non-cell based DPPH and ORAC assays. In HaCaT keratinocytes, irradiated with 226 J/cm2 UVA1 in low-serum (2%, starved) cell culture medium, pretreatment with 80 µM α-TP significantly enhanced cell survival (88%, Alamar Blue) compared to control, whereas α-T pre-treatment had no effect survival (70%, Alamar Blue). Pre-treatment of cells with 100 μM α-TP or 100 μM α-T before 57 J/cm2 UVA1 also significantly reduced ROS generation over 2 h (24.1% and 23.9% respectively) compared to the control and resulted in α-TP bioconversion into α-T. As α-TP displayed weak antioxidant activity in the cell-free assays thus its photoprotection was assigned to its bioconversion to α-T by cellular phosphatases. Through this mechanism α-TP prevented long-wave UVA1 induced cell death and scavenged UVA1 induced ROS in skin cells when added to the starved cell culture medium before UVA1 exposure by bioconversion into α-T.

Simultaneous NAD(P)H and FAD fluorescence lifetime microscopy of long UVA\u2013induced metabolic stress in reconstructed human skin

Solar ultraviolet longwave UVA1 exposure of human skin has short-term consequences at cellular and molecular level, leading at long-term to photoaging. Following exposure, reactive oxygen species (ROS) are generated, inducing oxidative stress that might impair cellular metabolic activity. However, the dynamic of UVA1 impact on cellular metabolism remains unknown because of lacking adequate live imaging techniques. Here we assess the UVA1-induced metabolic stress response in reconstructed human skin with multicolor two-photon fluorescence lifetime microscopy (FLIM). Simultaneous imaging of nicotinamide adenine dinucleotide (NAD(P)H) and flavin adenine dinucleotide (FAD) by wavelength mixing allows quantifying cellular metabolism in function of NAD(P)+/NAD(P)H and FAD/FADH2 redox ratios. After UVA1 exposure, we observe an increase of fraction of bound NAD(P)H and decrease of fraction of bound FAD indicating a metabolic switch from glycolysis to oxidative phosphorylation or oxidative stress possibly correlated to ROS generation. NAD(P)H and FAD biomarkers have unique temporal dynamic and sensitivity to skin cell types and UVA1 dose. While the FAD biomarker is UVA1 dose-dependent in keratinocytes, the NAD(P)H biomarker shows no dose dependence in keratinocytes, but is directly affected after exposure in fibroblasts, thus reflecting different skin cells sensitivities to oxidative stress. Finally, we show that a sunscreen including a UVA1 filter prevents UVA1 metabolic stress response from occurring.

UVA Exposure Combined with Glycation of the Dermis Are Two Catalysts for Skin Aging and Promotes a Favorable Environment to the Appearance of Elastosis.

Skin aging is the result of superimposed intrinsic (individual) and extrinsic (e.g., UV exposure or nutrition) aging. Previous works have reported a relationship between UV irradiation and glycation in the aging process, leading, for example, to modified radical species production and the appearance of AGEs (advanced glycosylation end products) in increasing quantities, particularly glycoxidation products like pentosidine. In addition, the colocalization of AGEs and elastosis has also been observed. We first investigated the combination of the glycation reaction and UVA effects on a reconstructed skin model to explain their cumulative biological effect. We found that UVA exposure combined with glycation had the ability to intensify the response for specific markers: for example, MMP1 or MMP3 mRNA, proteases involved in extracellular matrix degradation, or proinflammatory cytokine, IL1α, protein expression. Moreover, the association of glycation and UVA irradiation is believed to promote an environment that favors the onset of an elastotic-like phenomenon: mRNA coding for elastin, elastase, and tropoelastin expression is increased. Secondly, because the damaging effects of UV radiation in vivo might be more detrimental in aged skin than in young skin due to increased accumulation of pentosidine and the exacerbation of alterations related to chronological aging, we studied the biological effect of soluble pentosidine in fibroblasts grown in monolayers. We found that pentosidine induced upregulation of CXCL2, IL8, and MMP12 mRNA expression (inflammatory and elastotic markers, respectively). Tropoelastin protein expression (elastin precursor) was also increased. In conclusion, fibroblasts in monolayers cultured with soluble pentosidine and tridimensional in vitro skin constructs exposed to the combination of AGEs and UVA promote an inflammatory state and an alteration of the dermal compartment in relation to an elastosis-like environment.

Kinetic studies of photocatalytic degradation of an Azo dye by titania nanoparticles

Purpose Dyeing and printing are important steps in textile manufacturing. After the process completion, these dyes are released in the effluent. These dyes impart an unacceptable appearance but are also toxic to the soil and water bodies. The present research has been carried out to study the rate of photocatalytic degradation of an azo dye, namely, CI Direct Green 26, using titania nanoparticles under ultra violet (UV) irradiation as a function of temperature and time. Azo dyes account for the majority of all dyestuffs are produced and extensively used in the textile, paper, food, leather, cosmetics and pharmaceutical industries. Titania nanoparticles have been found to successfully degrade these dyes in the presence of UV light. The purpose of the present paper was to study the photodegradation of azo dyes using titania nanoparticles at different temperatures and time periods. Design/methodology/approach Titania nanoparticle concentration of 0.1% (w/v) was dispersed in distilled water by sonication for 1 h in sonication bath. The of rate of degradation of Direct Green 26 dye in the titania nanoparticle dispersion, under UV-A exposure was studied at different temperatures ranging from 25°C to 65 °C for time periods ranging from 1 h to 6 h. Photocatalytic degradation tests were performed in a specially designed UV reactor chamber. Raman spectroscopy of Titania nanoparticles, dye and titania/dye mixture before and after UV exposure was carried out using Confocal Laser Dispersion Raman Microscope (Renishaw, UK) with 785 nm excitation laser. Findings Titanium dioxide is an efficient photocatalyst for decolourisation of direct dye. The photodegradation of the direct Green dye was found to follow the pseudo first-order reaction. The Arrhenius activation energy was found to be 24.8 kJ/mol with A value of 0.0013 for the photocatalytic degradation of the dye. Raman spectroscopy also confirmed the adsorption of dye on titania nanoparticle and its complete degradation on exposure to UV light. Practical implications This research highlights the application of titania nanoparticles for the effective degradation of dye in the effluent from textiles, clothing, paper and any kind of dyeing process. Azo dyes account for the majority of all dyestuffs are produced and extensively used in the textile, paper, food, leather, cosmetics and pharmaceutical industries. Titania nanoparticles have been found to successfully degrade these dyes in the presence of UV light which can be very beneficial for the effluent treatment plants in textile and other industries. Originality/value Azo dyes are one of the harmful pollutants released in textile waste water. The degradation and removal of the coloured waste in the textile effluent is an important environmental concern and needs to be investigated. The research is one of the first to investigate and understand the mechanism of the degradation of an azo dye in the presence of titania nanoparticles by Raman spectroscopy.

343 A mixture of honeys and royal jelly to protect and repair Asian hair from UVA combined with environmental pollution

Medicine with natural bee products is getting more and more attention. Bee products have their activities on the skin proved by numerous studies and have been used in medical treatment and for cosmetic skin care. Each bee product possesses specific components which determine their activities. Honey contains more than 180 ingredients making each honey singular with unique properties. Beside carbohydrates, royal jelly contains among others amino acids, proteins, lipids, vitamins and is different from honey. Like skin, hair is exposed to UV and pollution causing oxidative damage such as protein carbonylation which lead to dull and brittle hair. The use of bee-products for hair care is poorly documented excepted for hair luster or conditioner. To investigate bee products hair care activities, we studied the protective and repair properties of a combination of 4 honeys from Ouessant, Corsica, Aland and Ikaria islands and a royal jelly (all with biological activities previously demonstrated) versus a stress generated by UVA exposure plus PM-10 (particle matter-10). Chinese hair shafts were stressed after or before the treatment with an aqueous solution of our bee product combination or with positive controls. After washing and drying, hair shafts were cryo-preserved, snap-frozen and cross-sectioned. Carbonylated proteins were labeled using a fluorescent probe functionalized with an aminooxy moiety. Following epi-fluorescence microscopy observations, analyses of cuticle and cortex areas were carried out with Image J software. Our bee products association allowed to protect hair shafts (cuticle by 100%, cortex by 94% versus control) and to repair them (cuticle by 99%, cortex by 82% versus control) from the aggression. For the first time with this original assay based on protein carbonylation on hair shafts, we have demonstrated the protective and repair activities of a bee products combination for hair, making this association a good candidate for hair care.

Tre-O2-08 - Phototherapy-induced interferon kappa drives type I interferon mediated anticancer responses in cutaneous T cell lymphoma

Phototherapy is a T cell immunosuppressive therapy that effectively treats inflammatory skin diseases and improves cutaneous T cell lymphoma by unclear mechanisms. We observed defective type I interferon production in untreated CTCL skin lesions. Effective tumor clearance was associated with upregulation of type I interferon production, increased recruitment of CD8 T cells into tumors and gene expression changes characteristic of antigen specific T cell activation. Malignant T cell numbers in skin were associated with increased expression of IRF2, a negative regulator of interferon production. Phototherapy increased gene and protein expression of interferon kappa, a UVB inducible up-regulator of type I interferon production. In vitro, UVA exposure induced production of interferon kappa by human keratinocytes that preceded upregulation of other type I interferons. Keratinocytes deficient in interferon kappa had decreased baseline and induced type I interferon expression in response to UVA. In summary, we find that phototherapy up regulates keratinocyte interferon kappa production, leading to enhanced type I interferon production and improved anticancer responses. These studies demonstrate a baseline deficit in type I interferon production in CTCL and suggest a role for interferon kappa in the mechanism of action of phototherapy.

Enhanced Ultraviolet Photoresponse Characteristics of Indium Gallium Zinc Oxide Photo-Thin-Film Transistors Enabled by Surface Functionalization of Biomaterials for Real-Time Ultraviolet Monitoring.

Indium gallium zinc oxide (IGZO) is one of the most promising materials for diverse optoelectronic applications based on thin-film transistors (TFTs) including ultraviolet (UV) photodetectors. In particular, the monitoring of UV-A (320-400 nm) exposure is very useful for healthcare applications because it can be used to prevent various human skin and eye-related diseases. However, the relatively weak optical absorption in the UV-A range and the persistent photoconductivity (PPC) arising from the oxygen vacancy-related states of IGZO thin films limit efficient UV monitoring. In this paper, we report the enhancement of the UV photoresponse characteristics of IGZO photo-TFTs by the surface functionalization of biomolecules on an IGZO channel. The biomaterial/IGZO interface plays a crucial role in enhancing UV-A absorption and suppressing PPC under negative gate bias, resulting in not only increased photoresponsivity and specific detectivity but also a fast and repeatable UV photoresponse. In addition, turning off the device without external bias completely eliminates PPC due to the internal electric field induced by the surface functionalization of biomaterials. Such a volatile feature of PPC enables the fast and repeatable UV photoresponse. These results suggest the potential of IGZO photo-TFTs combined with biomaterials for real-time UV monitoring.

Sensor surface via inspiration from Nature: The specific case of electron trapping in TiO2/WO3(∙0.33H2O) and reaction center/WO3(∙0.33H2O) systems

In this work, reaction center protein (RC) isolated from Rhodobacter sphaeroides purple bacteria was coupled with WO3(∙0.33H2O) via physical adsorption, where vectorial electron transfer (from RCs towards the inorganic carrier) was demonstrated using flash kinetics and photoluminescence measurements. The efficiency of the interaction between RCs and WO3(∙0.33H2O) was correlated to the components’ surface charge at the working pH and the structural/morphological and surface properties of the inorganic carrier (e.g., anchoring capacity assured by HO, WO bonds). The role of WO3(∙0.33H2O) as final electron trap and charge separator was proven not only in RCs/WO3(∙0.33H2O) biohybrid systems but also in TiO2/WO3(∙0.33H2O) composites. The charge transfer in the inorganic composites was evaluated by monitoring the reverse process of the color reaction (W5+ → W6+) via diffuse reflectance spectroscopy (DRS) after a previous UV-A (320–400 nm) exposure. The efficiency of the charge transfer process in inorganic systems was correlated to the initial W5+ content of WO3(∙0.33H2O), followed by the photocatalytic efficiency evaluation of these inorganic composites under UV-A irradiation.

Treating protracted corneal ulcers with UVA corneal collagen crosslinking: clinical cases

It has recently been proposed to use ultraviolet (UVA) corneal collagen crosslinking as an alternative method of treating bacterial ulcerative lesions of the cornea. Ambivalent results regarding the efficacy and safety of this method of treatment limit its implementation in clinical practice so far.The purpose of this work is to analyze three clinical cases involving the use of a new device for local UVA crosslinking in the complex treatment of bacterial corneal protracted-course ulcers with the suspected development of mixed fungal infection.Material and methods. For a dynamic follow-up of patients, we used biomicroscopy with a fluorescein test, photo registration and optical coherence tomography of the anterior part of the eye. Inflammatory changes were assessed using a point scale.Results. 3–5 procedures of local UVA exposure (with instillations of 0.1% riboflavin solution) lasting 3–5 minutes each and given with an interval of 2–4 days ensured stable and fast epithelialization of the cornea and a significant increase in visual acuity in the inflammatory process outcome.Conclusion. The first results of treating bacterial corneal ulcers using a new portable device for local UVA crosslinking have shown its high therapeutic efficiency and good prospects for further use in clinical practice.

Oxidative stress in the skin: Impact and related protection.

Skin, our first interface to the external environment, is subjected to oxidative stress caused by a variety of factors such as solar ultraviolet, infrared and visible light, environmental pollution, including ozone and particulate matters, and psychological stress. Excessive reactive species, including reactive oxygen species and reactive nitrogen species, exacerbate skin pigmentation and aging, which further lead to skin tone unevenness, pigmentary disorder, skin roughness and wrinkles. Besides these, skin microbiota are also a very important factor ensuring the proper functions of skin. While environmental factors such as UV and pollutants impact skin microbiota compositions, skin dysbiosis results in various skin conditions. In this review, we summarize the generation of oxidative stress from exogenous and endogenous sources. We further introduce current knowledge on the possible roles of oxidative stress in skin pigmentation and aging, specifically with emphasis on oxidative stress and skin pigmentation. Meanwhile, we summarize the science and rationale of using three well-known antioxidants, namely vitamin C, resveratrol and ferulic acid, in the treatment of hyperpigmentation. Finally, we discuss the strategy for preventing oxidative stress-induced skin pigmentation and aging.

Akt activation‐dependent protective effect of wild ginseng adventitious root protein against UVA‐induced NIH‐3T3 cell damage

Prolonged skin exposure to ultraviolet radiation can lead to development of several acute and chronic diseases, with UVA exposure considered a primary cause of dermal photodamage. We prepared a wild ginseng adventitious root extract (ARE) that could alleviate UVA irradiation-induced NIH-3T3 cell viability decline. After employing a series of purification methods to isolate main active components of ARE, adventitious root protein mixture (ARP) was identified then tested for protective effects against UVA irradiation-induced NIH-3T3 cell damage. The results showed that ARP treatment significantly reduced UVA-induced cell viability decline and confirmed that the active constituent of ARP was the protein, since proteolytic hydrolysis and heat treatment each eliminated ARP protective activity. Moreover, ARP treatment markedly inhibited UVA-induced apoptosis, cell cycle arrest and DNA fragmentation, while also significantly reversing UVA effects (elevated Bax levels, reduced Bcl-2 expression) by reducing Bax levels and increasing Bcl-2 expression. Mechanistically, ARP promoted Akt phosphorylation regardless of UVA exposure, thus confirming ARP resistance to inactivation by UVA light. Notably, in the presence of Akt inhibitor SC0227, ARP could no longer counteract UVA-induced cell viability decline and DNA fragmentation. Additionally, our results demonstrated that ARP treatment protected UVA-irradiated NIH-3T3 cells by preventing UVA-induced reduction of collagen-I expression. Taken together, these results suggest that ARP treatment of NIH-3T3 cells effectively mitigated UVA-induced cell viability decline by activating intracellular Akt to reduce UVA-induced DNA damage, leading to reduced rates of apoptosis and cell cycle arrest after UVA exposure and restoring collagen expression to normal levels.

Effects of UV and Heating on the Stability of Fucoxanthin, Total Phlorotannin and Total Antioxidant Capacities in Saccharina japonica Ethanol Extract and Solvent Fractions

The brown alga Saccharina japonica is widely consumed in Asian countries, and post-harvest drying methods such as sun drying and oven drying are commonly used to extend the shelf life of S. japonica. Thus, the present study analyzed the ethanol extract and organic solvent fractions of S. japonica to examine the effects of UVA and heating on certain bioactive compounds (fucoxanthin, phlorotannin compounds, and total antioxidants) during the drying process. The fucoxanthin contents in the ethanol extract and different solvent fractions significantly decreased in response to UVA. However, fucoxanthin in the ethanol extract and other fractions showed resistance to thermal treatment. It is noteworthy that the total phlorotannin content (TPC) in the ethanol extract and all fractions showed an approximately 2.5-fold increase upon UVA radiation. The TPC also increased in all samples exposed to high temperatures, except for those in the chloroform fraction. The total antioxidant capacity (TAC) also exhibited significant increases in a pattern similar to the TPC. The findings demonstrate that UVA exposure and heating stimulated the degradation of fucoxanthin while it increased the TPC and TAC in the extract and fractions of S. japonica.

An ex vivo model of human skin photoaging induced by UVA radiation compatible with summer exposure in Brazil.

Skin is the largest body organ and can be affected by several factors, such as ultraviolet (UV) radiation. UV radiation is subdivided in UVA, UVB and UVC according to the radiation wavelength. UVC radiation does not cross the ozone layer; UVB cause DNA damage and is closely related to carcinogenesis; UVA radiation penetrates deeply into the skin, reaching epidermis and dermis and is considered the main promoter of skin aging, known as photoaging. In order to understand photoaging mechanisms and propose efficient therapies, several photoaging study models have been developed, each with benefits and limitations, but most of them use very high doses of UVA radiation, which is not compatible with our daily sun exposure. The objective of this work was to develop a human ex vivo photoaging model induced by UVA exposure compatible to a summer in Brazil. For this, human skin fragments were obtained from healthy donors who underwent otoplasty surgery and skin explants were prepared and placed in plates, with the epidermis facing upwards. Skin explants were exposed to UVA at 16J/cm2 carried out by protocols of 2 or 4 exposures. Results showed an increase of oxidative damage, inflammatory cells, collagenolytic and elastolytic MMPs expression as well as a decrease of elastin expression, suggesting that the experimental model based on skin explants is able to evaluate UVA-induced aging in human skin.

Bellis perennis extract mitigates UVA-induced keratinocyte damage: Photoprotective and immunomodulatory effects.

A need exists for further research elucidating the benefits of environmentally safe photoprotective agents against ultraviolet (UV) exposure, and plant extracts represent a human-friendly alternative formulation. This study was designed to evaluate the potential use of Bellis perennis extract (BPE), from the Asteraceae family, known as the common daisy or the English daisy, in cosmeceuticals as a photoprotective factor, using an in vitro model of UVA-induced keratinocyte damage. Human skin keratinocytes (HaCaT cell line) were incubated with BPE at 0.01, 0.1, or 1% in Dulbecco's Modified Eagle Medium (DMEM), and after 15min they were submitted to UVA radiation at 5, 10, and 15J/cm2 doses, respectively. For comparative purposes, Polypodium leucotomos extract (PLE), known as the fern, was used as a positive control in assessing the photoprotective effect. After 24h of UVA exposure, cell viability (MTT and LDH assays), levels of cleaved caspase-3, cyclooxygenase-2, IL-6, reactive oxygen species (ROS) and antioxidant enzyme (catalase, SOD, and glutathione peroxidase) activity were determined. UVA radiation at 5, 10, and 15J/cm2 doses reduced cell viability to 63%, 43%, and 23%, respectively; we selected 10J/cm2 for our purposes. After 24h of UVA exposure, treatment with 1% BPE and 1% PLE significantly recovered cell viability (p<0.05). Furthermore, treatment was associated with lower cleaved caspase-3 and ROS levels, higher catalase activity, and lower IL-6 levels in the treated UVA keratinocytes compared with the untreated UVA group (p<0.01). Our results demonstrate photoprotective and immunomodulatory effects of BPE in skin keratinocytes and support its use as a bioactive agent in cosmetic formulations to prevent skin damage caused by exposure to the UV light.