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Purpose: Lycium barbarum polysaccharides (LBPs) have been proven to protect the eyes by inhibiting apoptosis. This study was designed to investigate the effect of LBPs on DNA damage and oxidative stress induced by ultraviolet B (UVB) radiation in human corneal epithelial cells (HCECs). Methods: HCECs were divided into a control group, UVB group and UVB + LBP group and treated with varying concentrations of LBP (0, 0.05, 0.1, 0.2, 0.4, 0.8, 1.6 and 3.2 mg/mL). Then, the effects of LBP on the viability and apoptosis of HCECs were detected via MTT assay and flow cytometry. Additionally, the contents of superoxide dismutase (SOD), malondialdehyde (MDA), and reactive oxygen species (ROS) in the cells of each group were measured to evaluate the level of oxidative stress. Results: LBP at a concentration of 0.4 mg/mL showed the best effect on promoting the viability and inhibiting the apoptosis of HCECs. Compared with the control group, the UVB and UVB + LBP groups exhibited significantly decreased levels of cell viability and SOD and notably increased apoptosis, MDA, ROS, tail DNA percentage, olive tail moment, p-CHK2, and gamma histone (γH2AX). In contrast to the UVB group, the UVB + LBP group presented notably upregulated levels of cell viability and SOD and downregulated apoptosis, MDA, ROS, tail DNA percentage, olive tail moment, p-CHK2, and γH2AX. Conclusions: The optimal concentration of LBP to promote the viability and reduce the apoptosis of HCECs is 0.4 mg/mL. Moreover, LBP can alleviate DNA damage and oxidative stress induced by UVB in HCECs. [ABSTRACT FROM AUTHOR]

The skin microenvironment created by keratinocytes (KC) influences the stress responses of melanocytes (MC) to UVB insults. This study employed RNA sequencing analysis as well as in vitro and in vivo models to elucidate the underlying mechanisms. Our RNA-Seq analysis revealed a statistically significant upregulation of GCSF and CCL20 genes in UVB-irradiated KC, correlating with the protective effects of KC on MC responses to UVB exposure. Recombinant GCSF and CCL20 exhibited the most pronounced modulation of UVB-induced MC responses. These effects included the attenuation of apoptosis and reduction of ROS formation, along with the upregulation of tyrosinase and tyrosinase-related protein-1, which are involved in the melanogenic pathway. ELISA was also used to confirm that UVB could induce the secretion of GCSF and CCL20 from KC. A similar correlation between GCSF and CCL20 expression in KC and tyrosinase levels in MC was observed in UVB-irradiated mouse skin. Our study provides novel insights into the protective role of GCSF and CCL20 in the paracrine effects of KC on UVB-induced MC damage through the modulation of stress response pathways, the MITF-tyrosinase axis, and the regulation of p53. These findings have implications for the development of pharmacological strategies targeting KC-derived paracrine factors for the prevention of skin photodamage. [ABSTRACT FROM AUTHOR]

Objective: Magnolia biondii, a plant containing many magnolian‐like compounds in its flowers or buds, exhibits anti‐inflammatory and antiallergic effects; however, no study has addressed its effect on alleviating ultraviolet light (UV)‐induced skin damage. We thus aimed at studying the effects of M. biondii flower extract (MB) on UVB‐induced skin damage and determine the relationship between cell damage and damage‐associated molecular patterns (DAMPs). Methods: Reconstructed epidermal models and foreskin samples were selected to detect cellular reactions after UVB irradiation and MB treatment. MTT, haematoxylin–eosin and immunofluorescence staining were used to examine total viability, sunburned cells and expression and migration of DAMPs at 16 or 48 h. Prostaglandin E2 (PGE‐2) and interleukin 8 (IL‐8) levels were measured using enzyme‐linked immunosorbent assays. A clinical UVB‐damaged test was carried out on human arms subjected to MB pre‐ or post‐treatment. Human skin probes were used to measure erythema, melanin, ITA° and transepidermal water loss (TEWL), while skin photos were captured using the VISIA system. Results: MB is rich in lignans such as magnolin, pinoresinol dimethyl ether and fargesin, and shows weak UV absorption at 280–320 nm. Coculturing with MB for 16 or 48 h after UVB irradiation improved the tissue viability and structure of Skinovo‐Epi, and reduced the expression and migration of high mobility group box protein B1 (HMGB1) as well as the expression of IL‐8 and PGE‐2. In the excised foreskin treated with MB after UVB irradiation, the generation of 8‐hidroxy‐2‐deoxyguanosine and nuclear transfer of HMGB1 were reduced. When pre‐treated with MB for 3 days, UVB‐induced skin erythema and ITA° were significantly decreased. When post‐treated with MB for 5 days, a decrease in skin erythema, melanin and TEWL values and an increase in skin ITA° were observed. Conclusions: Treatment with MB attenuated UVB‐induced skin damage, such as erythema, pigmentation and skin barrier function, by improving the tissue viability and structure and reducing sunburned cells and skin inflammation. This effect may be related to DNA damage, which causes the migration of HMGB1 from the nucleus to the outside of the cell to induce skin inflammation. [ABSTRACT FROM AUTHOR]

Key message: This study, using multi-omics combined with physiologic assays, found that calcium-ion signaling can regulate phenolic acid accumulation in R. chrysanthumleaves in response to UV-B stress. UV-B stress is a severe abiotic stress capable of destroying cellular structures and affecting plant growth. Rhododendron chrysanthum Pall. (R. chrysanthum) is a plant that has been exposed to high levels of UV-B radiation for an extended period, leading to the development of adaptive responses to mitigate UV-B stress. As such, it serves as a valuable experimental material for studying plant resilience to UV-B stress. We utilized R. chrysanthum as the experimental material and subjected it to UV-B stress. We conducted a comprehensive analysis of the changes in R. chrysanthum under both control and UV-B stress conditions using multi-omic and physiologic assays. Our aim was to investigate the molecular mechanism underlying R. chrysanthum’s resistance to UV-B stress, with a focus on calcium-ion signaling. UV-B stress was found to impact the photosynthesis of R. chrysanthum by decreasing the maximum photosynthetic efficiency of photosystem II, reducing Fm, and increasing F0. In addition, the composition of numerous phenolic acid compounds was significantly altered. Genes and proteins related to calcium signaling showed significant differences, with some proteins (CML, CPK1, CRK3, ATP2C, ERG3, CAR7) being modified by acetylation. The correlation between genes and proteins involved in calcium signaling and phenolic compounds suggested that calcium signaling may play a role in regulating the accumulation of phenolic compounds under UV-B stress to help R. chrysanthum adapt. This study examines the impact of calcium-ion signaling on the accumulation of phenolic acid compounds, offering insights for future research on the molecular mechanisms underlying plant resilience to UV-B stress. [ABSTRACT FROM AUTHOR]

Ultraviolet-B (UV-B) radiation overexposure causes function impairment of epidermal stem cells (ESCs). We explored the mechanism of Annexin A1 (ANXA1) ameliorating UV-B-induced ESC mitochondrial dysfunction/cell injury. ESCs were cultured in vitro and irradiated with different doses of UV-B. Cell viability/ANXA1 protein level were assessed. After oe-ANXA1 transfection, ESCs were treated with oe-ANXA1/UV-B irradiation/CCCP/CCG-1423/3-methyladenine for 12 h. Cell viability/death, and adenosine triphosphate (ATP)/reactive oxygen species (ROS) levels were determined. Mitochondrial membrane potential (MMP) changes/DNA (mtDNA) content/oxygen consumption and RhoA activation were assessed. ROCK1/p-MYPT1/MYPT1/(LC3BII/I)/Beclin-1/p62 protein levels were determined. Mitochondrial morphology was observed. Mito-Tracker Green (MTG) and LC3B levels were determined. UV-B irradiation decreased cell viability/ANXA1 expression in a dose-dependent manner. UV-B-treated ESCs exhibited reduced cell viability/ATP content/MMP level/mitochondrial respiratory control ratio/mtDNA number/RhoA activity/MYPT1 phosphorylation/MTG+LC3B+ cells/(LC3BII/I) and Beclin-1 proteins, increased cell death/ROS/p62/IL-1β/IL-6/TNF-α expression, contracted mitochondrial, disappeared mitochondrial cristae, and increased vacuolar mitochondria, which were averted by ANXA1 overexpression, suggesting that UV-B induced ESC mitochondrial dysfunction/cell injury/inflammation by repressing mitophagy, but ANXA1 promoted mitophagy by activating the RhoA/ROCK1 pathway, thus repressing UV-B’s effects. Mitophagy activation ameliorated UV-B-caused ESC mitochondrial dysfunction/cell injury/inflammation. Mitophagy inhibition partly diminished ANXA1-ameliorated UV-B’s effects. Conjointly, ANXA1 promoted mitophagy by activating the RhoA/ROCK1 pathway, thereby improving UV-B-induced ESC mitochondrial dysfunction/cell injury. [ABSTRACT FROM AUTHOR]

This study aims to investigate the hypothesis that Yes‐associated protein (YAP) significantly regulates antioxidant potential and anti‐apoptosis in UVB‐induced cataract by exploring the underlying molecular mechanisms. To investigate the association between YAP and cataract, various experimental techniques were employed, including cell viability assessment, Annexin V FITC/PI assay, measurement of ROS production, RT‐PCR, Western blot assay, and Immunoprecipitation. UVB exposure on human lens epithelium cells (HLECs) reduced total and nuclear YAP protein expression, increased cleaved/pro‐caspase 3 ratios, decreased cell viability, and elevated ROS levels compared to controls. Similar Western blot results were observed in in vivo experiments involving UVB‐treated mice. YAP knockdown in vitro demonstrated a decrease in the protein expression of FOXM1, Nrf2, and HO‐1, which correlated with the mRNA expression, accompanied by an increase in cell apoptosis, caspase 3 activation, and the release of ROS. Conversely, YAP overexpression mitigated these effects induced by UVB irradiation. Immunoprecipitation revealed a FOXM1‐YAP interaction. Notably, inhibiting FOXM1 decreased Nrf2 and HO‐1, activating caspase 3. Additionally, administering the ROS inhibitor N‐acetyl‐L‐cysteine (NAC) effectively mitigated the apoptotic effects induced by oxidative stress from UVB irradiation, rescuing the protein expression levels of YAP, FOXM1, Nrf2, and HO‐1. The initial findings of our study demonstrate the existence of a feedback loop involving YAP, FOXM1, Nrf2, and ROS that significantly influences the cell apoptosis in HLECs under UVB‐induced oxidative stress. [ABSTRACT FROM AUTHOR]

Copyright of China Surfactant Detergent & Cosmetics (2097-2806) is the property of China Surfactant Detergent & Cosmetics Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Protecting the skin from the effects of UVB radiation using natural products is crucial in the cosmeceutical industry. This study aims to investigate the protective effects of Bangle (Zingiber cassumunar Roxb.) against UVB‐induced skin damage in Wistar albino rats. The rhizomes were macerated using 70% ethanol v/v, followed by n‐hexane to obtain n‐hexane soluble and n‐hexane insoluble fraction. The antioxidant properties of the ethanol extracts and n‐hexane soluble fraction were evaluated using a 2,2‐diphenyl‐1‐picrylhydrazyl (DPPH) assay. The study also examined the antiphotoaging properties through reactive oxygen species (ROS) scavenging assay, matrix metalloproteinase‐1 (MMP‐1) expression, and tyrosinase expression against UVB radiation in Wistar albino rats. The results demonstrated that the Z. cassumunar extract and fraction effectively converted DPPH radicals into a more stable compound. Analysis revealed the presence of Benzene, 4‐(1Z)‐1,3‐butadien‐1‐yl‐1,2‐dimethoxy‐ and (E)‐4‐(3,4‐Dimethoxyphenyl) but‐3‐en‐1‐ol as the primary compounds in both the extract and fraction, suggesting their contribution to the observed activity. Furthermore, Z. cassumunar compounds could reduce UVB‐induced ROS production and may protect against skin photoaging by changing the expression of MMP‐1 and tyrosinase levels in Wistar albino rats. These findings suggest that Z. cassumunar holds promise for preventing skin aging.

Cholinergic urticaria is a dermatological disease characterized by the presence of large patches of red skin and transient hives triggered by factors, such as exercise, sweating, and psychological tension. This skin problem is hypothesized to be attributed to a reduced expression of acetylcholinesterase (AChE), an enzyme responsible for hydrolyzing acetylcholine (ACh). Consequently, ACh is thought to the leak from sympathetic nerves to skin epidermis. The redundant ACh stimulates the mast cells to release histamine, triggering immune responses in skin. Here, the exposure of ultraviolet B in skin suppressed the expression of AChE in keratinocytes, both in in vivo and in vitro models. The decrease of the enzyme was resulted from a declined transcription of ACHE gene mediated by micro‐RNAs, that is, miR‐132 and miR‐212. The levels of miR‐132 and miR‐212 were markedly induced by exposure to ultraviolet B, which subsequently suppressed the transcriptional rate of ACHE. In the presence of low level of AChE, the overflow ACh caused the pro‐inflammatory responses in skin epidermis, including increased secretion of cytokines and COX‐2. These findings suggest that ultraviolet B exposure is one of the factors contributing to cholinergic urticaria in skin. [ABSTRACT FROM AUTHOR]

Cornulin (CRNN) and repetin (RPTN) belong to the fused‐type S100 protein family. Although these proteins have been reported to be expressed in the granular layer of the epidermis and have been suggested to be associated with barrier formation in the epidermis, their exact function remains unclear. This study examined the effects of ultraviolet B (UVB) irradiation on CRNN and RPTN expression in human skin xenotransplantation. The CRNN expression increased in the granular layer of UVB‐irradiated skin 2 days after UVB irradiation compared to that in sham‐irradiated skin. Interestingly, CRNN signals were observed not only in the cytoplasm, but also in the peripheral regions of granular keratinocytes. In contrast, RPTN was rarely expressed in sham‐irradiated skin; however, RPTN signals were markedly increased in the granular layer of the UVB‐irradiated skin. In addition, activation of ERK1/2 and STAT3 was observed in UVB‐irradiated skin. Accordingly, the present study demonstrated that CRNN and RPTN are novel proteins whose expression can be increased by UVB irradiation. The activation of ERK1/2 and STAT3 may be associated with the regeneration of a UVB‐damaged epidermis, and CRNN and RPTN may be induced to repair any dysfunction in the epidermal barrier during this regeneration process. [ABSTRACT FROM AUTHOR]

Copyright of China Surfactant Detergent & Cosmetics (2097-2806) is the property of China Surfactant Detergent & Cosmetics Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Skin aging is affected by a variety of factors, including ultraviolet rays, oxidative stress, medications, smoking, and genetics. Among them, photo-aging accounts for about 80% of skin aging. The present study was evaluated to verify the potential of Allomyrina dichotoma larvae, which has recently been attracting attention as an edible insect, as an anti-aging substance. UVB irradiation at 100 mJ/cm2 was sufficient to induce photo-aging of fibroblasts within 24 h, which was alleviated after treatment with 70% ethanol extract of Allomyrina dichotoma larvae extract (ADLE). To obtain an extract from ADLE, which has a relatively high content of polyphenol compounds containing physiological activity, fractional solvent extraction was carried out using organic solvents such as hexane, chloroform, ethyl acetate, and butanol. Additionally, ethyl acetate and butanol fractions contributed to the inhibition of UVB-induced ROS production, cell damage, and senescence of fibroblasts. It was also confirmed that the two fractions can regulate the expression of MMP-1 and AP-1. In particular, the ethyl acetate fraction showed an excellent effect in recovering collagen decomposed by UVB. Therefore, these results suggest that ADLE has potential as a natural insect-derived biomaterial to inhibit UVB-induced photo-aging.

The skin microenvironment created by keratinocytes (KC) influences the stress responses of melanocytes (MC) to UVB insults. This study employed RNA sequencing analysis as well as in vitro and in vivo models to elucidate the underlying mechanisms. Our RNA-Seq analysis revealed a statistically significant upregulation of GCSF and CCL20 genes in UVB-irradiated KC, correlating with the protective effects of KC on MC responses to UVB exposure. Recombinant GCSF and CCL20 exhibited the most pronounced modulation of UVB-induced MC responses. These effects included the attenuation of apoptosis and reduction of ROS formation, along with the upregulation of tyrosinase and tyrosinase-related protein-1, which are involved in the melanogenic pathway. ELISA was also used to confirm that UVB could induce the secretion of GCSF and CCL20 from KC. A similar correlation between GCSF and CCL20 expression in KC and tyrosinase levels in MC was observed in UVB-irradiated mouse skin. Our study provides novel insights into the protective role of GCSF and CCL20 in the paracrine effects of KC on UVB-induced MC damage through the modulation of stress response pathways, the MITF-tyrosinase axis, and the regulation of p53. These findings have implications for the development of pharmacological strategies targeting KC-derived paracrine factors for the prevention of skin photodamage.

Canola meal, a by-product of canola oil processing, is a source of bioactive compounds that show antioxidant and skin anti-aging effects through upcycling (i.e., creative reuse). Here we describe the antioxidant and skin anti-aging effects of canola meal extract (CME) obtained by upcycling canola meal. The antioxidant capacity of CME is due in part to its antioxidative phenolics. Seven phenolics, including sinapine and sinapic acid, in CME were identified using ultra-high-performance liquid chromatography–Orbitrap mass spectrometry. Addition of CME (1000 μg/mL) to human dermal fibroblast neonatal cells significantly (p < 0.05) reduced matrix metalloproteinase-12 production and increased pro-collagen Ι alpha 1 content in response to ultraviolet B-induced oxidative stress compared with cells without CME. These results suggest that CME can serve as a functional food ingredient with antioxidant capacity and anti-aging effects on the skin. [ABSTRACT FROM AUTHOR]

Summary: Legume nodulation requires light perception by plant shoots and precise long‐distance communication between shoot and root. Recent studies have revealed that TGACG‐motif binding factors (GmSTFs) integrate light signals to promote root nodulation; however, the regulatory mechanisms underlying nodule formation in changing light conditions remain elusive.Here, we applied genetic engineering, metabolite measurement, and transcriptional analysis to study soybean (Glycine max) nodules.We clarify a fine‐tuning mechanism in response to ultraviolet B (UV‐B) irradiation and rhizobia infection, involving GmUVR8‐dependent UV‐B perception and GmSTF3/4‐GmMYB12‐GmCHS‐mediated (iso)flavonoid biosynthesis for soybean nodule formation. GmUVR8 receptor‐perceived UV‐B signal triggered R2R3‐MYB transcription factors GmMYB12‐dependent flavonoid biosynthesis separately in shoot and root. In shoot, UV‐B‐triggered flavonoid biosynthesis relied on GmUVR8a, b, c receptor‐dependent activation of GmMYB12L‐GmCHS8 (chalcone synthase) module. In root, UV‐B signaling distinctly promotes the accumulation of the isoflavones, daidzein, and its derivative coumestrol, via GmMYB12B2‐GmCHS9 module, resulting in hypernodulation. The mobile transcription factors, GmSTF3/4, bind to cis‐regulatory elements in the GmMYB12L, GmMYB12B2, and GmCHS9 promoters, to coordinate UV‐B light perception in shoot and (iso)flavonoid biosynthesis in root.Our findings establish a novel shoot‐to‐root communication module involved in soybean nodulation and reveal an adaptive strategy employed by soybean roots in response to UV‐B light. [ABSTRACT FROM AUTHOR]

Copyright of China Surfactant Detergent & Cosmetics (2097-2806) is the property of China Surfactant Detergent & Cosmetics Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Kangfuxin liquid (KFX), an extract of the American cockroach, has been clinically proven to be effective in various skin damage disorders, but there are no reports on its use in photodamage. We explored the effect of KFX on ultraviolet B (UVB)-induced photodamage and whether its mechanism was related to autophagy. We found that KFX treatment reduced UVB-induced reactive oxygen species production and improved the vitality of cells inhibited by UVB irradiation. The expression of LC3 (A/B), which was inhibited after UVB irradiation, could be rescued by KFX treatment. Furthermore, KFX may upregulate the level of cellular autophagy by regulating the AMPK-mTOR signaling pathway. When the autophagy inhibitor wortmannin was used to inhibit autophagy, the protective effect of KFX on cells was diminished or even disappeared. Our study suggests that KFX may resist UVB-mediated oxidative stress damage of HaCaT through the induction of autophagy. [ABSTRACT FROM AUTHOR]

The human eye, constantly exposed to solar radiation, can be damaged by UV radiation. In particular, ultraviolet B (UVB)-induced damage plays an important role in retinal degeneration and cell aging. In this study, we investigated the protective effects of the methanol extract of Oxya chinensis sinuosa (OCM), an edible insect known for its high protein content (64.2%), and various pharmacological effects, on human retinal pigment epithelial cells. ARPE-19 cells were treated with OCM and subsequently UVB irradiated. Our results showed that OCM effectively attenuates UVB-induced cell damage by reducing MAPK phosphorylation (JNK and p38 MAPK). Additionally, OCM increased the phosphorylation of Akt, and cell cycle regulators, including p21 and p27, in a dose-dependent manner. Moreover, OCM treatment increased ARPE-19 cell proliferation by activating the S6K1/S6 pathway. This study suggests that OCM prevents UVB-induced retinal cell damage by increasing cell proliferation via ROS reduction, suggesting its potential as a functional therapeutic superfood against retinal cell damage. [ABSTRACT FROM AUTHOR]

Ultraviolet (UV) irradiation has been identified as a key trigger for skin photoaging, characterized by the overproduction of matrix metalloproteinases (MMPs) and reactive oxygen species (ROS), along with the accelerated decomposition of extracellular matrix (ECM) proteins, ultimately contributing to the development of wrinkles. Persicaria senticosa (PS) extracts are recognized for their antioxidative properties and their importance in skin health. Nevertheless, there is a paucity of studies investigating the potential of PS in protecting the skin against photoaging. The present study aimed to assess the effectiveness of PS extracts in preventing photoaging and elucidating the molecular mechanisms involved in using immortalized human keratinocytes (HaCaT) and hairless mice. The major bioactive constituents of PS were identified as p-coumaric acid, isoquercitrin, quercetin-3-O-glucuronide, and quercetin. Aqueous extracts of PS exhibited the ability to mitigate UVB-induced cellular damage and diminished ROS generation in HaCaT cells. Moreover, treatment with PS effectively attenuated the upregulated expression of matrix metalloproteinase-1 (MMP-1) and collagen degradation induced by UVB exposure. The property of PS to counteract photoaging was related to its capacity to inhibit the UVB-induced phosphorylation of mitogen-activated protein kinase (MAPK) and suppress the subsequent activation of activator protein 1 (AP-1) signaling pathways. Moreover, in hairless mice exposed to UVB radiation, the application of PS significantly alleviated the development of skin wrinkles, diminished epidermal thickening, and mitigated collagen degradation. Notably, PS treatment resulted in the downregulation of the UVB-activated MAPK/AP-1/MMP-1 pathway in mouse skin tissues. These findings suggest that PS has the potential to serve as a therapeutic agent for treating photoaging, holding promises in both cosmeceutical and pharmaceutical applications.

Abstract Background The different wavelengths of solar radiation incident on earth [herein: Photosynthetically Active Radiation (PAR) , Ultra Violet-A (UV-A) and Ultra Violet-B (UV-B)] and their spectral balance not only have an impact on plants’ growth, morphology and physiology, but also are important for the quality and quantity of plant secondary metabolites. Material and methods In an outdoor study we addressed the effects of PAR intensity and UV-A and UV-B on the growth, yield, phenolic and flavonoid content, antioxidant activity and essential oil composition of Pelargonium graveolens L’Hér. The experiment was performed with split plots in a randomized complete block design with three replications. During the growth, two PAR intensities (ambient PAR and reduced PAR) and four UV treatments (ambient UV, enhanced UV-A, enhanced UV-B and enhanced UVA + B) were applied. Results High PAR intensity decreased the length and width of leaf, the height of plant and fresh weight of aerial parts, and increased the dry weight of aerial parts. Enhanced UV-B irradiation was associated with reduced plant height, leaf expansion and fresh and dry weight of aerial parts. Interestingly, the negative effect of UV-B radiation on morphology and growth of plant was largely alleviated by high PAR intensity. The amount of total phenols and flavonoids, antioxidant activity and essential oil production of P. graveolens strongly increased with the increase of UV-B irradiation and PAR. On the other hand, UV-A radiation did not significantly influence total phenol and flavonoid content, antioxidant activity and essential oil composition. Moreover, the combination of high PAR intensity and UV-B led to further increases in total flavonoid content and antioxidant capacity. Both high PAR intensity and enhanced UV-B increased the percentage of geraniol in essential oil, leading to a slight reduction of citronellol/geraniol ratio which is a marker of quality for rose geranium essential oil. Conclusions Overall, we conclude that UV-B irradiation was associated to reduction of plant growth and yield, while, the adverse effect of UV-B irradiation on the plant was mitigated by high PAR intensity. On the other hand, both high PAR and enhanced UV-B boosted the production of phenols, flavonoids and essential oil. Considering that the lower citronellol/geraniol ratio is the most important indicator for the economic value of rose geranium essential oil, reducing citronellol/geraniol ratio under enhanced UV-B radiation and/or high PAR is likely to be favorable.

Background Ultraviolet B (UV‐B) irradiation is an effective treatment for human cutaneous disorders and was shown to reduce experimental atherosclerosis by attenuating immunoinflammatory responses. The aim of this study was to clarify the effect of specific wavelengths of UV‐B on atherosclerosis and the underlying mechanisms focusing on immunoinflammatory responses. Methods and Results Based on light‐emitting diode technology, we developed novel devices that can emit 282 nm UV‐B, which we do not receive from natural sunlight, 301 nm UV‐B, and clinically available 312 nm UV‐B. We irradiated 6‐week‐old male atherosclerosis‐prone Apoe−/− (apolipoprotein E‐deficient) mice with specific wavelengths of UV‐B and evaluated atherosclerosis and immunoinflammatory responses by performing histological analysis, flow cytometry, biochemical assays, and liquid chromatography/mass spectrometry‐based lipidomics. Irradiation of 282 nm UV‐B but not 301 or 312 nm UV‐B significantly reduced the development of aortic root atherosclerotic plaques and plaque inflammation. This atheroprotection was associated with specifically augmented immune responses of anti‐inflammatory CD4+ Foxp3 (forkhead box P3)+ regulatory T cells in lymphoid tissues, whereas responses of other immune cells were not substantially affected. Analysis of various lipid mediators revealed that 282 nm UV‐B markedly increased the ratio of proresolving to proinflammatory lipid mediators in the skin. Conclusions We demonstrated that 282 nm UV‐B irradiation effectively reduces aortic inflammation and the development of atherosclerosis by systemically augmenting regulatory T‐cell responses and modulating the balance between proresolving and proinflammatory lipid mediators in the skin. Our findings indicate that a novel 282 nm UV‐B phototherapy could be an attractive approach to treat atherosclerosis.

Background: The different wavelengths of solar radiation incident on earth [herein: Photosynthetically Active Radiation (PAR) , Ultra Violet-A (UV-A) and Ultra Violet-B (UV-B)] and their spectral balance not only have an impact on plants' growth, morphology and physiology, but also are important for the quality and quantity of plant secondary metabolites. Material and methods: In an outdoor study we addressed the effects of PAR intensity and UV-A and UV-B on the growth, yield, phenolic and flavonoid content, antioxidant activity and essential oil composition of Pelargonium graveolens L'Hér. The experiment was performed with split plots in a randomized complete block design with three replications. During the growth, two PAR intensities (ambient PAR and reduced PAR) and four UV treatments (ambient UV, enhanced UV-A, enhanced UV-B and enhanced UVA + B) were applied. Results: High PAR intensity decreased the length and width of leaf, the height of plant and fresh weight of aerial parts, and increased the dry weight of aerial parts. Enhanced UV-B irradiation was associated with reduced plant height, leaf expansion and fresh and dry weight of aerial parts. Interestingly, the negative effect of UV-B radiation on morphology and growth of plant was largely alleviated by high PAR intensity. The amount of total phenols and flavonoids, antioxidant activity and essential oil production of P. graveolens strongly increased with the increase of UV-B irradiation and PAR. On the other hand, UV-A radiation did not significantly influence total phenol and flavonoid content, antioxidant activity and essential oil composition. Moreover, the combination of high PAR intensity and UV-B led to further increases in total flavonoid content and antioxidant capacity. Both high PAR intensity and enhanced UV-B increased the percentage of geraniol in essential oil, leading to a slight reduction of citronellol/geraniol ratio which is a marker of quality for rose geranium essential oil. Conclusions: Overall, we conclude that UV-B irradiation was associated to reduction of plant growth and yield, while, the adverse effect of UV-B irradiation on the plant was mitigated by high PAR intensity. On the other hand, both high PAR and enhanced UV-B boosted the production of phenols, flavonoids and essential oil. Considering that the lower citronellol/geraniol ratio is the most important indicator for the economic value of rose geranium essential oil, reducing citronellol/geraniol ratio under enhanced UV-B radiation and/or high PAR is likely to be favorable. [ABSTRACT FROM AUTHOR]

Although it is well recognized that mycosporine-like amino acids (MAAs) are ultraviolet (UV) protective agents that can reduce UV damage, the specific biological mechanism of its role in the skin remains unclear. In this study, we investigated the effect of MAAs extracted from Antarctic diatom Phaeodactylum tricornutum ICE-H on UVB-induced skin damage using a mice model. The MAAs components identified by liquid chromatography-tandem mass spectrometry included 4-deoxygadusol, shinorine, and porphyra-334, which were purified using a Supledean Carboxen1000 solid phase extraction column. The antioxidant activities of these MAA compounds were tested in vitro. For UVB-induced skin photodamage in mice, MAAs alleviated skin swelling and epidermal thickening in this study. We detected the content of reactive oxygen species (ROS), malondialdehyde, and collagen in skin tissue. In addition, quantitative real-time polymerase chain reaction was used to detect nuclear factor-κB (NF-κB), tumor necrosis factor α, interleukin-1β, cyclooxygenase-2, mitogen activated protein kinase (MAPK) family (extracellular signal-regulated kinase, c-Jun amino-terminal kinase, and p38 kinase), and matrix metalloproteinases. The expression of these cytokines and enzymes is related to inflammatory responses and collagen degradation. In comparison to the model group without MAA treatment, the MAA component decreased the concentration of ROS, the degree of oxidative stress in the skin tissue, and the expression of genes involved in the NF-κB and MAPK pathways. In summary, these MAA components extracted from Phaeodactylum tricornutum ICE-H protected against UVB-induced skin damage by inhibiting ROS generation, relieving skin inflammation, and slowing down collagen degradation, suggesting that these MAA components are effective cosmetic candidate molecules for the protection and therapy of UVB damage. [ABSTRACT FROM AUTHOR]

Background: UV exposure is one of the primary factors responsible for photoaging, causing the increase in matrix metalloproteinases (MMPs) and the reduction in collagen. Salvia plebeia R. Br (SP), as an herbaceous plant, contains abundant flavonoids and possesses excellent anti‐inflammatory and antioxidant activities. This study aimed to investigate the photoprotective effects of SP on UVB‐induced photodamage in immortalized human keratinocytes (HaCaTs) and Kunming mice, as well as its main active components such as homoplantaginin (HP). Methods: CCK‐8 was applied to detect the cell viability in UVB‐irradiated or non‐irradiated HaCaTs. Commercial kits were used to evaluate the levels of ROS, MDA, SA‐β‐Gal, MMP‐1, and IL‐6. The expression of MAPK and TGF‐β/Smad pathways was detected by western blot. HE and Masson's trichrome staining were performed to examine the epidermis thickness and collagen degradation of Kunming mice. Results: Our results found that SP and HP notably decreased UVB‐induced ROS, MDA, and SA‐β‐Gal production, and inhibited MMP‐1 and IL‐6 secretion by inhibiting the MAPK signaling pathway. In addition, SP and HP significantly promoted type I procollagen synthesis by activation of TGF‐β/Smad pathway. Consistently, the in vivo experiments also indicated that SP and HP had a photoprotective effect, which significantly reversed UVB‐induced epidermis thickness and collagen degradation. Conclusion: This study demonstrated that SP effectively could protect skin from UVB‐induced photoaging, while HP acted as the active substance in SP. All these findings provided a new strategy for skin photoaging treatment. [ABSTRACT FROM AUTHOR]

Cataracts, a prevalent age-related eye condition, pose a significant global health concern, with rising rates due to an aging population and increased digital device usage. In Taiwan, cataract prevalence is particularly high, reaching up to 90% among individuals aged 70 and above. The lens of the eye absorbs short-wave light, which can lead to oxidative stress in lens epithelial cells and contribute to cataract formation. Exposure to ultraviolet (UV) light further exacerbates the risk of cataracts by generating reactive oxygen species. Heat-shock proteins (HSPs), involved in protein maintenance and repair, have been linked to cataract development. Cordyceps cicadae (C. cicadae), a traditional Chinese medicine, has a long history of use and is known for its pharmacological effects. N6-(2-hydroxyethyl) adenosine (HEA), a bioactive compound found in C. cicadae, exhibits anti-inflammatory, immunomodulatory, and neuroprotective properties. Previous studies have shown that C. cicadae mycelial extracts improve dry eye disease and reduce intraocular pressure in animal models. Additionally, C. cicadae possesses antioxidant properties, which are beneficial for combating cataract formation. In this study, we aim to evaluate the preventive efficacy of C. cicadae mycelial extracts in UV-induced cataract development. By investigating the ameliorative effects of C. cicadae on eye diseases and its potential role in ocular health improvement, we hope to uncover new options for cataract prevention and provide insights into the mechanisms of action. The findings of this research could provide a novel approach for nutritional supplements targeting cataract prevention, offering potential benefits in the field of ocular health. [ABSTRACT FROM AUTHOR]

The purpose of this study was to illuminate the mechanism by which Schizonepeta tenuifolia Briq. (ST) ethanolic extract prevents skin photoaging in HR-1 hairless mice (HR-1). The ST ethanolic extract alleviated wrinkle formation, epidermal skin thickness, and collagen degradation in skin tissues of ultraviolet B (UVB)-irradiated HR-1 mice. Expression of matrix metalloproteinases (a wrinkle-related marker) was reduced, and tissue inhibitor of metalloproteinase 1 expression was upregulated following application of ST ethanolic extract. Furthermore, skin dehydration and levels of hyaluronidase-1 and -2 (enzymes that break hyaluronic acid) were decreased. Moreover, protein expression of hyaluronan synthases (markers of skin hydration) and hyaluronic acid levels increased following ST ethanolic extract treatment in UVB-induced photoaging HR-1 mice. In addition, the phosphorylation of mitogen-activated protein kinases (MAPKs), including p38, extracellular signal-regulated kinase, and Jun N-terminal kinase was suppressed, and expression of nuclear factor-kappa was reduced. Treatment with ST ethanolic extract also reduced advanced glycation end product (AGE) accumulation and expression of the receptor for AGE (RAGE) in skin tissue. These results suggest that ST ethanolic extract moderates skin damage caused by UVB irradiation via regulating the expression of wrinkle- and hydrationrelated proteins, MAPKs, and RAGE. [ABSTRACT FROM AUTHOR]

Ultraviolet B (UVB) exposure is reported to cause cataract formation by inducing excessive reactive oxygen species (ROS) and apoptosis in human lens epithelial cells (HLECs). Sodium-dependent Vitamin C transports-2 (SVCT2) is a ascorbic acid (AsA) transporter for that can protect cells and tissues from oxidative stress. Here, we focus on the functional characterization and mechanism analysis of SVCT2 in UVB-treated HLECs. The results showed a significant reduction of SVCT2 expression in HLECs treated with UVB. SVCT2 abated apoptosis and Bax expression and increased Bcl-2 expression. Moreover, SVCT2 decreased ROS accumulation and MDA level, but increased the activities of antioxidant enzymes (SOD and GSH-PX). NF-κB inhibitor (PDTC) alleviated ROS production and apoptosis, and promoted SVCT2 expression in UVB-treated HLECs. Additionally, ROS inhibitor (NAC) suppressed oxidative stress, apoptosis, and induced SVCT2 expression in UVB-treated HLECs, while these effects were significantly abated due to the activation of NF-κB signaling. Furthermore, SVCT2 facilitated 14C-AsA absorption in UVB-treated HLECs. Together, our findings demonstrated that UVB exposure-induced ROS generation, which further activated NF-κB signaling to down-regulate SVCT2 expression in HLECs. Then, downregulated SVCT2 promoted ROS accumulation and induced apoptosis by decreasing AsA uptake. Our data reveal a novel NF-κB/SVCT2/AsA regulatory pathway and suggest the therapeutic potential of SVCT2 in UVB-induced cataract. [ABSTRACT FROM AUTHOR]

As a promising environmental protection technology, the application of ultraviolet B irradiation in vegetable production has been widely considered. However, the effect of UVB irradiation varies with different plant varieties. In this study, we investigated the effects of two UVB intensities (0.7, 1.4 W m−2) on the accumulation of phenolics and flavonoids, and antioxidant activity of green-leaf and red-leaf lettuce (Lactuca sativa L.) 7 days prior to harvest. The results indicated that short-term (within 2 days) UVB treatment could promote the increase in total chlorophyll content of red-leaf lettuce and green-leaf lettuce, which increased by 49.8% and 20.6% compared with day zero, respectively, and was beneficial to the synthesis of carotenoids of red-leaf lettuce. Extending UVB exposure time significantly decreased chlorophyll a/b value of green-leaf lettuce from 0.92 to 0.63, and simultaneously increased the accumulation of antioxidant substances such as flavonoids, which were increased by 90.0% and 183.4% compared with day zero for UVB-0.7 and UVB-1.4 treatments of red-leaf lettuce, 84.1% and 110.9% of green-leaf lettuce. In contrast, red-leaf lettuce had a higher accumulation level of secondary metabolites, faster scavenging rate of free radicals, and stronger ability to resist UVB stress. Our results suggest that supplementation of low-dose UVB radiance prior to harvest can improve the secondary metabolite content and antioxidant activity of the two kinds of lettuce. This research provided a theoretical basis for improving lettuce quality by pre-harvest UVB treatment in controlled environmental agriculture. [ABSTRACT FROM AUTHOR]

Ultraviolet (UV) is the main cause of sunburn on the skin as it induces erythema and accelerates pigmentation. Vitamin C is one of the most frequently used compounds to reduce UV-induced skin pigmentation, but it has limitations in absorption through the skin. In this study, we tested whether a no-ozone cold plasma (NCP) treatment can improve UV-irradiated skin by helping the action of Vitamin C. For this, among five groups of HRM-2 hairless mice, four groups of mice were subjected to UVB irradiation, and three groups of UVB-treated mice were treated with NCP, Vitamin C, and NCP + Vitamin C, respectively. For evaluating the effect of each treatment, the melanin and erythema index was measured during animal experiments. Histological changes were monitored by performing H&E and MTS and IHC against tyrosinase and melanin. As a result, the naturally recovered mice showed a 28-point decrease in the melanin index, whereas a decrease of around 88, 74.3, and 106 points was detected in NCP-, Vitamin C-, and NCP + vitamin C-treated mice, respectively. Likewise, only a 39-point reduction in the erythema index was monitored in naturally recovered mice, but the NCP-, vitamin C-, and NCP + vitamin C-treated mice showed a 87.3-, 77-, and 111-point reduction, respectively. Interestingly, the skin tissues of the mice treated with NCP in combination with Vitamin C mostly recovered from UVB-induced damage. Altogether, this study elucidated the beneficial effect of the treatment of NCP in combination with Vitamin C on the UVB-irradiated skin, which might be helpful for treating sunburn on the skin. [ABSTRACT FROM AUTHOR]

The effect of supplemental lighting on strawberry growth and anthracnose disease response of three strawberry (Fragaria ×ananassa) cultivars was evaluated in two greenhouse trials, and the effect on strawberry anthracnose pathogens (Colletotrichum sp.) was evaluated in the laboratory. The objective of the greenhouse trials was to determine the effect of various intensities of the red and blue light emitting diode (LED) light treatment on strawberry plant vigor, injury, and disease development. In these trials, the duration of supplemental light treatments was split into two 4-hour periods: dawn and dusk. The intensity of the red and blue LED bulbs was set using an adjustable dial at 1 or 3 in trial 1 and at 1, 5, or 10 in trial 2. Illuminance and photosynthetic photon flux densities of the light treatments ranged from lows of 402 lx and 5 μmol⋅m–2⋅s–1 (blue LED 1) to highs of 575 lx and 25 μmol⋅m–2⋅s–1 (red LED 1 + blue LED 3) in trial 1, and from lows of 4213 lx and 81 μmol⋅m–2⋅s–1 (red LED 1) to highs of 7051 lx (red LED 5) and 194 μmol⋅m–2⋅s–1 (red LED 10) in trial 2. Lower light intensities in trial 1 resulted in no significant differences as a result of light treatments in relative chlorophyll content, plant vigor ratings, or disease severity ratings (DSRs). However, plant injury ratings were significantly greater in plants in the wide-spectrum fluorescent (WSF) plus ultraviolet B (UVB) light treatment compared with the other treatments. Under the higher light intensities in trial 2, there were more significant effects among light treatments. Relative chlorophyll content of plants in the WSF + UVB, WSF, and red LED 1 treatments was significantly greater than that of plants in the red LED 10 treatment; however, plants in the red LED 10 treatment had the greatest injury ratings. Detached leaves from plants in the red 5 LED and red 10 LED treatments inoculated with Colletotrichum gloeosporioides received the greatest DSRs, and leaves from plants in the red LED 1 and WSF treatments received the lowest DSRs. In the laboratory, five days of exposure to supplemental lights did not prevent the growth of isolates of three species of Colletotrichum pathogens even though the intensity of the LED lights was set at their highest intensity. However, growth of isolates exposed to the WSF + UVB light treatment was slowed.

Liwen Wang,1,&ast; Guangmei Wan,1,&ast; Gang Wang,1 Meihong Zhang,1 Nanxin Li,1 Qinning Zhang,2 Hualing Yan1 1Department of Dermatology, Qinghai University Affiliated Hospital, Xining, People’s Republic of China; 2Shijingshan Teaching Hospital, Capital Medical University, Beijing, People’s Republic of China&ast;These authors contributed equally to this workCorrespondence: Hualing Yan, Department of Dermatology, Qinghai University Affiliated Hospital, No. 29, Tongren Road, Chengxi District, Xining, Qinghai Province, People’s Republic of China, Email yhlckw@163.comPurpose: The study aimed to investigate the potential protective role of anthocyanin from Lycium ruthenicum Murr. in the Qaidam Basin against ultraviolet B (UVB)-induced apoptosis of human skin fibroblasts (HSFs).Methods: HSFs cultured in vitro were randomly divided into a control group, UVB group, and anthocyanin groups (0.1, 0.5, and 1.0 mg/mL). HSFs in the UVB and anthocyanin groups were exposed to 30 mJ/cm2 UVB to establish a photoaging model. Then, apoptosis rate, tumor necrosis factor-α (TNF-α), cysteinyl aspartate specific proteinase-3 (caspase-3), cysteinyl aspartate specific proteinase-7 (caspase-7), and survivin expression were evaluated.Results: UVB irradiation can increase the apoptosis rate of HSFs and expression of TNF-α, caspase-7, and survivin. Anthocyanin pretreatment (0.1, 0.5, and 1.0 mg/mL) decreased UVB-induced apoptosis rate and TNF-α and caspase-7 expression and increased survivin expression. Compared with the control group, the apoptosis rate and expression of TNF-α, caspase-7, and survivin of anthocyanin groups in UVB-irradiated HSFs were high. Among the three doses of anthocyanin (0.1, 0.5, and 1.0 mg/mL) groups, the apoptosis rate and TNF-α expression of anthocyanin at 1.0 mg/mL were the lowest. There was no significant change in caspase-3 expression in each group.Conclusion: Anthocyanin from Lycium ruthenicum Murr. in the Qaidam Basin could alleviate UVB-induced apoptosis by regulating the death receptor pathway.Keywords: Lycium ruthenicum Murr., anthocyanin, human skin fibroblasts, ultraviolet B, apoptosis

UVB exposure accelerates skin aging and pigmentation. Melatonin effectively regulates tyrosinase (TYR) activity and aging. The purpose of this study was to determine the association between premature senescence and pigmentation, and the mechanism of melanin synthesis effected by melatonin. Primary melanocytes were extracted and identified from the male foreskin. To inhibit TYR expression, primary melanocytes were transduced with the lentivirus pLKD-CMV-EGFP-2A-Puro-U6-TYR. The wild-type TYR(+/+) and TYR(–/–) or TYR(+/–) knockout C57BL/6 J mice were used to determine the role of TYR on melanin synthesis in vivo. Results showed that UVB-induced melanin synthesis is dependent on TYR in primary melanocytes and mice. Furthermore, in primary melanocytes pretreated with Nutlin-3 or PFT-α to up or downregulate p53, results showed that premature senescence and melanin synthesis increased in primary melanocytes after UVB irradiation at 80 mJ/cm2, and further increased after being treated with Nutlin-3, while significantly decreased with PFT-α. In addition, melatonin inhibited UVB-induced premature senescence associated with inactivation of p53 and phosphorylation of p53 on Ser15 (ser-15), a decrease of melanin synthesis accompanied by reduced TYR expression. Moreover, skin erythema and pigmentation induced by UVB were reduced in the dorsal and ear skin of mice topically pretreated with 2.5% melatonin. These indicate that melatonin inhibits UVB-induced senescence-associated pigmentation via the p53-TYR pathway in primary melanocytes and prevents pigmentation obviously in the dorsal and ear skin of C57BL/6 J mice after UVB irradiation. Key messages: P53 links UVB irradiation-induced senescence and senescence-associated pigmentation and regulates TYR in primary melanocytes after UVB irradiation. Melatonin inhibits senescence-associated pigmentation through the p53-TYR pathway in primary melanocytes. Melatonin prevents skin erythema and melanin pigmentation induced by UVB irradiation in the dorsal and ear skin of C57BL/6J mice. [ABSTRACT FROM AUTHOR]

An unripe apple (immature fruit of Malus pumila Mill) contains more polyphenols than mature fruit. To explore the anti-photoaging effects of unripe apple extract (UAE), we investigated the effects of UAE on wrinkle improvement, skin moisturizing, skin inflammation, and antioxidant activities using the ultraviolet B (UVB)-irradiated SKH1-hr hairless mouse model. The mice were irradiated with UVB (0.18 J/cm2) three times per week and orally administrated UAE (100, 200, or 400 mg/kg) once a day for 15 weeks. The administration of UAE significantly prevented UVB-induced wrinkle formation and skin water loss, potentially by increasing the effects of UAE on type I collagen (COL1) and hyaluronic acid through the transcriptional regulation of COL1α (COL1A1 and COL1A2), hyaluronan synthesis (HAS1, HAS2, and HAS3) and the matrix metalloproteinase (MMP1, MMP9, and MMP13) gene. Moreover, UAE significantly reduced UVB-induced skin edema, infiltrated neutrophils, and pro-inflammatory cytokine interleukin-1β (IL-1β), while increasing the anti-inflammatory cytokine IL-10. UAE also exerted anti-oxidative stress properties by increasing the glutathione content and inhibiting lipid peroxidation and superoxide anion production. The histopathological analysis demonstrated that UAE-induced anti-inflammation, anti-oxidative stress, and anti-apoptotic properties on the UVB-irradiated skin tissues. Therefore, UAE may be an effective natural resource to mitigate UVB-induced skin photoaging. [ABSTRACT FROM AUTHOR]

Hyperpigmentation stimulated by ultraviolet (UV)-induced melanin overproduction causes various cosmetic problems. UV radiation's activation of the cyclic adenosine monophosphate (cAMP)-mediated cAMP-dependent protein kinase (PKA)/cAMP response element-binding protein (CREB)/microphthalmia-associated transcription factor (MITF) pathway is the main pathway for melanogenesis. However, the secretion of adenosine triphosphate (ATP) from keratinocytes due to UV radiation also leads to melanogenesis. Adenosine, converted from ATP by CD39 and CD73, can activate adenylate cyclase (AC) activity and increase intracellular cAMP expression. cAMP-mediated PKA activation results in dynamic mitochondrial changes that affect melanogenesis via ERK. We evaluated whether radiofrequency (RF) irradiation could decrease ATP release from keratinocytes and suppress the expression of CD39, CD73, and A2A/A2B adenosine receptors (ARs) and the activity of AC and downregulate the PKA/CREB/MITF pathway, which would eventually decrease melanogenesis in vitro in UV-irradiated cells and animal skin. Our results indicate that RF decreased ATP release from UVB-irradiated keratinocytes. When conditioned media (CM) from UVB-irradiated keratinocytes (CM-UVB) were administered to melanocytes, the expressions of CD39, CD73, A2A/A2BARs, cAMP, and PKA increased. However, the expression of these factors decreased when CM from UVB and RF-irradiated keratinocytes (CM-UVB/RF) was administered to melanocytes. The phosphorylation of DRP1 at Ser637, which inhibits mitochondrial fission, increased in UVB-irradiated animal skin and was decreased by RF irradiation. The expression of ERK1/2, which can degrade MITF, was increased using RF treatment in UVB-irradiated animal skin. Tyrosinase activity and melanin levels in melanocytes increased following CM-UVB administration, and these increases were reversed after CD39 silencing. Tyrosinase activity and melanin levels in melanocytes were decreased by CM-UVB/RF irradiation. In conclusion, RF irradiation decreased ATP release from keratinocytes and the expressions of CD39, CD73, and A2A/A2BARs, which decreased AC activity in melanocytes. RF irradiation downregulated the cAMP-mediated PKA/CREB/MITF pathway and tyrosinase activity, and these inhibitory effects can be mediated via CD39 inhibition. [ABSTRACT FROM AUTHOR]

The skin is constantly exposed to exogenous environmental stressors and has to cope with excessive oxidative stress and tissue damage. However, exposure to moderate environmental stressors may be beneficial for the cutaneous tissue and assist in protecting against oxidative damage via the enhanced activation of the nuclear factor erythroid 2‐related factor 2–Kelch‐like ECH‐associated protein 1 (Nrf2–Keap1) pathway. Such moderate stressors can be found in various locations around the globe. In this manuscript, we chose to focus on the Dead Sea (DS) area as a test case to study the effect of moderate stressors on the cutaneous tissue because of the unique combinations of moderate stressors in this area. The exceptional location of the DS at an altitude of −438 meters below sea level (the lowest place on earth) is responsible for its rare accumulation of moderate stressors such as high‐water salinity, high atmospheric pressure, and unique solar radiation. In this manuscript, we hypothesized that the unique solar radiation in the DS area generates moderate oxidative stress in the skin leading to the induction of intracellular electrophiles, which in turn can activate the protecting Nrf2‐Keap1 pathway. We showed that exposure of human skin organ culture from the same donor to solar radiation at the DS resulted in significant activation of the Nrf2‐Keap1 pathway, induction of phase II enzymes, and lower apoptotic activity compared to a nearby location at a higher altitude (Jerusalem +700 m). This remarkable effect of activating the Nrf2 protecting pathway and the importance and characteristics of the solar irradiation at the DS is discussed. [ABSTRACT FROM AUTHOR]

Introduction: C-phycocyanin (C-PC), a photosynthetic protein obtained from Spirulina, is regarded a highly promising commercially available biochemical. Numerous in vitro and in vivo studies have provided evidence of C-PC’s ability to mitigate the inflammatory response, alleviate oxidative stress, and facilitate wound healing. However, despite the existing knowledge regarding C-PC’s protective mechanism against cellular apoptosis induced by ultraviolet B (UVB) radiation, further in vivo experiments are needed to explore its anti-photoaging mechanism.Methods: In this study, a UVB-induced skin photoaging model was established using BALB/c-nu mice, and the potential protective effects of topically administered c-PC were investigated by various molecular biology tools. In addition, a novel delivery system, C-PC nanodispersion, was developed to facilitate the transdermal delivery of C-PC.Results: C- PC demonstrated significant anti-photoaging activities in the UVB-induced skin. The application of C-PC to the dorsal skin of the mice resulted in improved macroscopic characteristics, such as reduced sagging and coarse wrinkling, under UVB irradiation Histological analyses showed that C-PC treatment significantly decreased the symptoms of epidermal thickening, prevented dermal collagen fiber loosening, increased the hydroxyproline (Hyp) content and activities of antioxidant enzymes (such as superoxide dismutase, catalase, and glutathione peroxidase) in mouse skin, decreased malondialdehyde levels and expressions of inflammatory factors (interleukin-1α [IL-1α], IL-1β, IL-6, and tumor necrosis factor-α), reduced matrix metalloproteinase [MMP-3 and MMP-9] expressions, and inhibited the phosphorylation of c-Jun N-terminal kinase, extracellular signal-regulated kinase, and p38 proteins in the mitogen-activated protein kinase family.Discussion: By analyzing the results of the study, a new drug delivery system, C-PC nano-dispersion, was proposed, and the anti-photoaging effect of C-PC and its mechanism were investigated.

We recently reported that exposure of skin to ultraviolet B (UVB) irradiation for 2 weeks induces stress and accelerates skin aging. Interestingly, aldosterone synthase is known to be crucial in generating UVB-induced stress-related responses, suggesting that drugs that regulate its activity can be used as skin antiaging agents. Through extensive drug screening, we have identified 20-hydroxyecdysone (20E), a steroidal prohormone secreted by the prothoracic glands of insects, as a potent inhibitor of UVB-induced aging. Although 20E has been shown to exert antistress and anti-collagenase effects in vitro, its effects in vivo remain unexplored. Furthermore, the pharmacological and physiological effects of 20E on UVB-mediated photoaging are poorly understood. Therefore, in this study, we investigated the effects of 20E on aldosterone synthase and UVB-induced photoaging and skin lesions in hairless mice, focusing on the stress-related hypothalamic–pituitary–adrenal axis. We confirmed that 20E inhibited aldosterone synthase and reduced corticosterone levels. When applied to a UV-induced skin aging animal model, it ameliorated UV-induced stress and protected against the decrease in collagen levels. Importantly, when the aldosterone synthase inhibitor osilodrostat, an FDA-approved drug, was applied to the UV-induced skin aging model, the stress-reducing and antiaging effects of 20E were not observed. Thus, we conclude that 20E inhibits UVB-induced skin aging by blocking aldosterone synthase and is a potential candidate to prevent skin aging.

Khairuddin Djawad,1 Irawan Yusuf,2 Upik Anderiani Miskad,3 Ilhamjaya Jaya Patellongi,4 Muhammad Nasrum Massi5 1Department of Dermatology and Venereology, Hasanuddin University, Makassar, South Sulawesi, Indonesia; 2Department of Pathological Anatomy, Hasanuddin University, Makassar, South Sulawesi, Indonesia; 3Department of Physiology and Biostatics, Hasanuddin University, Makassar, South Sulawesi, Indonesia; 4Department of Physiology, Hasanuddin University, Makassar, South Sulawesi, Indonesia; 5Department of Medical Microbiology, Hasanuddin University, Makassar, South Sulawesi, IndonesiaCorrespondence: Khairuddin Djawad, Email duddin@ymail.comBackground: Ultraviolet B (UVB) exposure leads to formation of photoproducts leading to cellular damage. Prevention using sunscreen can sometimes be inadequate and can be an economic burden. Recent studies have suggested the photoprotective effect of curcumin.Objective: To examine the acute and chronic photoprotective effect of topical curcumin, using cyclobutyl pyrimidine dimers (CPD) and 8-hydroxy2ʹdeoxyguanosine (8-OHdG) expression as markers of DNA-induced damage, and epidermal hyperplasia on UVB-induced mice.Methods: Three treatment groups were established. Group A (negative control) consisted of 5 mice, Group B and C were further divided into two categories to assess acute and chronic effects of topical curcumin and UVB radiation. Each consisted of six subgroups of five mice. Subgroup 1; UVB exposure only (positive control) subgroup 2; acetone and UVB exposure, subgroup 3– 6; topical curcumin application of 100nM, 1μM, 10μM, and 100μM concentrations, respectively. In Group C, there were two categories that received 3x/week UVB exposure for three weeks which effects were being observed at 24 hours and 10 days after the last exposure. The topical curcumin dose was 2mg/mL/cm2 applied 30 minutes prior to 343mJ/cm2/day UVB irradiation. Skin biopsy was done one hour after the last UVB exposure for immunohistochemical and histopathology examinations.Results: Topical curcumin showed a limited yet robust protective effect against CPD and 8-OHdG expression in Group B, while in Group C all concentrations showed significant CPD and 8-OHdG inhibition after 10 days of UVB exposure. The 10μM and 100μM concentrations showed the best epidermal hyperplasia inhibition effect (p< 0.05). No significant differences were found in terms in efficacy either in single nor daily application.Conclusion: Topical curcumin can prevent the formation of the photoproducts CPD and 8-OHdG and epidermal hyperplasia in both acute and chronic exposure in UVB-induced mice.Keywords: curcumin, cyclobutyl pyrimidine dimers, 8-hydroxy2ʹdeoxyguanosine, epidermal hyperplasia, ultraviolet B, UVB, CPD

Powdery mildew and two-spotted spider mite are detrimental to strawberry plants and are controlled with traditional pesticides. To accommodate consumer demand, eco-friendly methods of pest control are required. Strawberries were cultivated (in soil and in a hydroponic system) for two years, and ultraviolet B (UV-B) irradiation was used as an alternative pest control during the harvesting season. Three varieties were grown (Seolhyang, Kingsberry, and Durihyang), and four UV-B lamp/mulch (black, green, and light reflection sheet [LRS]) combinations were used during harvesting: UV-B+black or green mulch, UV-B+black or green+LRS, no UV-B+black or green, and no UV-B+black or green+LRS. In all varieties, powdery mildew was 65% more controlled when UV-B irradiation was used. The adult two-spotted spider mite density was lowest in the UV-B lamp+black or green+LRS treatments. Therefore, UV-B irradiation during the strawberry harvesting season could effectively control powdery mildew and two-spotted spider mite with little side effect on the plants.

Ultraviolet (UV) B exposure induces wrinkle formation, collagen fiber breakdown, and transepidermal water loss (TEWL). UVB irradiation induces the expression of mitogen-activated protein kinase (MAPK), activator protein 1 (AP-1), and nuclear factor kappa B (NF-κB), which affect the expression of matrix metalloproteinases (MMP). We confirmed the effects of Latilactobacillus sakei wikim0066 (wikim0066) on UVB-irradiated Hs68 cells and HR-1 hairless mice cells. wikim0066 restored the production of type I procollagen by regulating the expression of MMP-1 and -3, MAPK, AP-1, and NF-κB in UVB-irradiated Hs68 cells and HR-1 mice. Oral administration of wikim0066 alleviates wrinkle formation, epidermal thickness, and TEWL in UVB-irradiated HR-1 hairless mice. These results indicated that wikim0066 has the potential to prevent UVB-induced wrinkle formation. [ABSTRACT FROM AUTHOR]

The effect of supplemental lighting on strawberry growth and anthracnose disease response of three strawberry (Fragaria ×ananassa) cultivars was evaluated in two greenhouse trials, and the effect on strawberry anthracnose pathogens (Colletotrichum sp.) was evaluated in the laboratory. The objective of the greenhouse trials was to determine the effect of various intensities of the red and blue light emitting diode (LED) light treatment on strawberry plant vigor, injury, and disease development. In these trials, the duration of supplemental light treatments was split into two 4-hour periods: dawn and dusk. The intensity of the red and blue LED bulbs was set using an adjustable dial at 1 or 3 in trial 1 and at 1, 5, or 10 in trial 2. Illuminance and photosynthetic photon flux densities of the light treatments ranged from lows of 402 lx and 5 lmol·m–2 ·s –1 (blue LED 1) to highs of 575 lx and 25 lmol·m–2 ·s –1 (red LED 1 1 blue LED 3) in trial 1, and from lows of 4213 lx and 81 lmol·m–2 ·s –1 (red LED 1) to highs of 7051 lx (red LED 5) and 194 lmol·m–2·s –1 (red LED 10) in trial 2. Lower light intensities in trial 1 resulted in no significant differences as a result of light treatments in relative chlorophyll content, plant vigor ratings, or disease severity ratings (DSRs). However, plant injury ratings were significantly greater in plants in the wide spectrum fluorescent (WSF) plus ultraviolet B (UVB) light treatment compared with the other treatments. Under the higher light intensities in trial 2, there were more significant effects among light treatments. Relative chlorophyll content of plants in the WSF 1 UVB, WSF, and red LED 1 treatments was significantly greater than that of plants in the red LED 10 treatment; however, plants in the red LED 10 treatment had the greatest injury ratings. Detached leaves from plants in the red 5 LED and red 10 LED treatments inoculated with Colletotrichum gloeosporioides received the greatest DSRs, and leaves from plants in the red LED 1 and WSF treatments received the lowest DSRs. In the laboratory, five days of exposure to supplemental lights did not prevent the growth of isolates of three species of Colletotrichum pathogens even though the intensity of the LED lights was set at their highest intensity. However, growth of isolates exposed to the WSF 1 UVB light treatment was slowed. [ABSTRACT FROM AUTHOR]

In this study, the co-culture system of Caco-2 and HaCaT cells was established, and the inhibitory effect of punicalagin on cyclobutene pyrimidine dimers (CPD) which was one major type of UVB-induced DNA lesions was evaluated by immunofluorescence. Then the effects of punicalagin on transcription and expression levels of nucleotide excision repair (NER) related genes was further investigated by quantitative real-time PCR, immunoprecipitation and western-blotting. The results showed that punicalagin reduced CPD level in HaCaT cells, upregulated xeroderma pigmentosum group C (XPC) mRNA level and attenuated XPA acetylation in a SIRT1-dependent manner. This showed, punicalagin's efficacy against UVB-induced photodamage in the co-culture system of Caco-2 and HaCaT cells was probably activated by the NER related XPC/ XPA which depended on the deacetylation activity of SIRT1. [ABSTRACT FROM AUTHOR]

Sinapate esters, which are induced in plants under ultraviolet-B (UV-B) irradiation, have important roles not only in the protection against UV-B irradiation but also in the regulation of stomatal closure. Here, we speculated that sinapate esters would function in the stomatal closure of Arabidopsis thaliana in response to UV-B. We measured the stomatal aperture size of the wild-type (WT) and bright trichomes 1 (brt1) and sinapoylglucose accumulator 1 (sng1) mutants under UV-B irradiation; the latter two mutants are deficient in the conversion of sinapic acid to sinapoylglucose (SG) and SG to sinapoylmalate (SM), respectively. Both the brt1 and sng1 plants showed smaller stomatal apertures than the WT under normal light and UV-B irradiation conditions. The accumulation of SM and malate were induced by UV-B irradiation in WT and brt1 plants but not in sng1 plants. Consistently, exogenous malate application reduced UV-B-induced stomatal closure in WT, brt1 and sng1 plants. Nonetheless, levels of reactive oxygen species (ROS), nitric oxide (NO) and cytosolic Ca2+ were higher in guard cells of the sng1 mutant than in those of the WT under normal white light and UV-B irradiation, suggesting that disturbance of sinapate metabolism induced the accumulation of these signaling molecules that promote stomatal closure. Unexpectedly, exogenous sinapic acid application prevented stomatal closure of WT, brt1 and sng1 plants. In summary, we hypothesize that SG or other sinapate esters may promote the UV-B-induced malate accumulation and stomatal closure, whereas sinapic acid inhibits the ROS-NO pathway that regulates UV-B-induced cytosolic Ca2+ accumulation and stomatal closure. [ABSTRACT FROM AUTHOR]

Objectives: To explore the short‐ and long‐term effects of UVB phototherapy preceding a fractional CO2 laser‐UVB protocol in patients with resistant nonsegmental vitiligo. Materials and Methods: This single‐center, prospective, split‐face/body, evaluator‐blinded study included adult patients with stable vitiligo refractory to conventional treatments. Two symmetrical lesions were selected. Phototherapy was delivered with one side covered, until minimal erythema. Within 3 days, 31‐month‐apart sessions of laser were performed on both sides. After each laser session, phototherapy was resumed three times weekly, with all lesions uncovered, until 8 weeks after the last laser session. At baseline, at the end of treatment, and 5 years later, a Mean Improvement Score by Physician (MISP) and a patient satisfaction 10‐point visual analog score (VAS) were recorded. Results: Ten patients (8 women and 2 men) were included; their mean age was 32.9 years; phototype III was predominant; the mean duration of vitiligo was 3 years. At the end of treatment and 5 years later, scores of lesions treated with UVB‐CO2‐UVB (mean MISP 3.0 and 2.9, mean ΔVAS 4.5 and 3.9, respectively), were higher than those of lesions treated only with CO2‐UVB (mean MISP 2.5 and 2.4, mean ΔVAS 4.1 and 3.6, respectively). After 5 years, one patient lost his partial response and two patients developed light hyperpigmentation on both sides. Conclusion: Exposure to UVB before CO2‐UVB explains the higher scores as it was the only variable between the two sides. It may improve the response of resistant lesions with a constantly sustained result over 5 years. [ABSTRACT FROM AUTHOR]

Ultraviolet B (UVB) exposure causes a breakdown of collagen, oxidative stress, and inflammation. UVB activates mitogen-activated protein kinase (MAPK), activator protein-1 (AP-1), and matrix metalloproteinases (MMPs). In this study, we evaluated 2,2′-azino-bis-(3-ethylbenzothiazoline-6-sulfonic acid) (ABTS+) radical scavenging activity and the photoprotective effect of lactic acid bacteria LAB strains, including Lactobacillus, Bifidobacterium, and Streptococcus genera in UVB-exposed skin fibroblasts. Nine LAB strains displayed antioxidant activity by regulating superoxide dismutase in UVB-exposed skin fibroblasts. Four LAB strains (MG4684, MG5368, MG4511, and MG5140) recovered type I procollagen level by inhibiting MMPs, MAPK, and AP-1 protein expression. Additionally, these four strains reduced the expression of proinflammatory cytokines by inhibiting oxidative stress. Therefore, L. fermentum MG4684, MG5368, L. rhamnosus MG4511, and S. thermophilus MG5140 are potentially photoprotective. [ABSTRACT FROM AUTHOR]

Skin photoaging, which causes wrinkles, increased epidermal thickness, and rough skin texture, is induced by ultraviolet B (UVB) exposure. These symptoms by skin photoaging have been reported to be involved in the reduction of collagen by the expression of matrix metalloproteinases (MMPs) and activator protein-1 (AP-1). This study investigated the protective effects of Bifidobacterium animalis subsp. lactis MG741 (Bi. lactis MG741) in Hs-68 fibroblasts and hairless mice (HR-1) following UVB exposure. We demonstrated that the Bi. lactis MG741 reduces wrinkles and skin thickness by downregulating MMP-1 and MMP-3, phosphorylation of extracellular signal-regulated kinase (ERK), and c-FOS in fibroblasts and HR-1. Additionally, in UVB-irradiated dorsal skin of HR-1, Bi. lactis MG741 inhibits the expression of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), an inflammation-related factor. Thus, Bi. lactis MG741 has the potential to prevent wrinkles and skin inflammation by modulating skin photoaging markers. [ABSTRACT FROM AUTHOR]

Repetitive exposure to ultraviolet B (UVB) is one of the main causes of skin photoaging. We previously reported that dieckol isolated from Eisenia bicyclis extract has potential anti-photoaging effects in UVB-irradiated Hs68 cells. Here, we aimed to evaluate the anti-photoaging activity of dieckol in a UVB-irradiated hairless mouse model. In this study, hairless mice were exposed to UVB for eight weeks. At the same time, dieckol at two doses (5 or 10 mg/kg) was administered orally three times a week. We found that dieckol suppressed UVB-induced collagen degradation and matrix metalloproteinases (MMPs)-1, -3, and -9 expression by regulating transforming growth factor beta (TGF-β)/Smad2/3 and mitogen-activated protein kinases (MAPKs)/activator protein-1 (AP-1) signaling. In addition, dieckol rescued the production of hyaluronic acid (HA) and effectively restored the mRNA expression of hyaluronan synthase (HAS)-1/-2 and hyaluronidase (HYAL)-1/-2 in UVB-irradiated hairless mice. We observed a significant reduction in transepidermal water loss (TEWL), epidermal/dermal thickness, and wrinkle formation in hairless mice administered dieckol. Based on these results, we suggest that dieckol, due to its anti-photoaging role, may be used as a nutricosmetic ingredient for improving skin health. [ABSTRACT FROM AUTHOR]

Abstract Background Chronic exposure to ultraviolet B (UVB) causes a series of adverse skin reactions, such as erythema, sunburn, photoaging, and cancer, by altering signaling pathways related to inflammation, oxidative stress, and DNA damage. Marine algae have abundant amounts and varieties of bioactive compounds that possess antioxidant and anti-inflammatory properties. Thus, the objective of this study was to investigate the photoprotective effects of an ethanol extract of Sargassum thunbergii. Methods Sargassum thunbergii phenolic-rich extract (STPE) was prepared, and its activity against UVB damage was evaluated using L929 fibroblast cells and zebrafish. STPE was extracted and purified by 40% ethanol and macroporous resin XDA-7. Reactive oxygen species (ROS) and antioxidant markers, such as superoxide dismutase (SOD), catalase (CAT) activities, and malondialdehyde (MDA) content were analyzed. The effect of STPE on UVB-induced inflammation was determined by inflammatory cytokine gene and protein expression. The expression of signaling molecules in the Nuclear Factor KappaB (NF-κB) pathway was determined by western blotting. DNA condensation was analyzed and visualized by Hoechst 33342 staining. In vivo evaluation was performed by tail fin area and ROS measurement using the zebrafish model. Results The total polyphenol content of STPE was 72%. STPE reduced ROS content in L929 cells, improved SOD and CAT activities, and significantly reduced MDA content, thereby effectively alleviating UVB radiation-induced oxidative damage. STPE inhibited the mRNA and protein expression of TNF-α, IL-6, and IL-1α. STPE reversed DNA condensation at concentrations of 20 and 40 μg/mL compared with the UVB control. Moreover, STPE inhibited NF-κB signaling pathway activation and alleviated DNA agglutination in L929 cells after UVB irradiation. Additionally, 1.67 μg/mL STPE significantly increased the tail fin area in zebrafish, and 0.8–1.6 μg/mL STPE effectively eliminated excessive ROS after UVB radiation. Conclusions STPE inhibited UVB-induced oxidative stress, inflammatory cytokine expression, and DNA condensation via the downregulation of the NF-κB signaling pathway, suggesting that it prevents UVB-induced photodamage, and has potential for clinical development for skin disease treatment.

Although it is well recognized that mycosporine-like amino acids (MAAs) are ultraviolet (UV) protective agents that can reduce UV damage, the specific biological mechanism of its role in the skin remains unclear. In this study, we investigated the effect of MAAs extracted from Antarctic diatom Phaeodactylum tricornutum ICE-H on UVB-induced skin damage using a mice model. The MAAs components identified by liquid chromatography-tandem mass spectrometry included 4-deoxygadusol, shinorine, and porphyra-334, which were purified using a Supledean Carboxen1000 solid phase extraction column. The antioxidant activities of these MAA compounds were tested in vitro. For UVB-induced skin photodamage in mice, MAAs alleviated skin swelling and epidermal thickening in this study. We detected the content of reactive oxygen species (ROS), malondialdehyde, and collagen in skin tissue. In addition, quantitative real-time polymerase chain reaction was used to detect nuclear factor-κB (NF-κB), tumor necrosis factor α, interleukin-1β, cyclooxygenase-2, mitogen activated protein kinase (MAPK) family (extracellular signal-regulated kinase, c-Jun amino-terminal kinase, and p38 kinase), and matrix metalloproteinases. The expression of these cytokines and enzymes is related to inflammatory responses and collagen degradation. In comparison to the model group without MAA treatment, the MAA component decreased the concentration of ROS, the degree of oxidative stress in the skin tissue, and the expression of genes involved in the NF-κB and MAPK pathways. In summary, these MAA components extracted from Phaeodactylum tricornutum ICE-H protected against UVB-induced skin damage by inhibiting ROS generation, relieving skin inflammation, and slowing down collagen degradation, suggesting that these MAA components are effective cosmetic candidate molecules for the protection and therapy of UVB damage.