Search Results (259)

Background: Ultraviolet B (UVB) radiation accelerates skin aging by inducing oxidative stress, collagen degradation, and cellular senescence. Although Petasites japonicus is known for its antioxidant properties, its anti-photoaging potential remains underexplored. This research explored the protective properties of a hot water extract from P. japonicus leaves (KP-1) against photoaging caused by UVB exposure. Methods: Hairless mice were exposed to UVB three times per week and orally administered KP-1 for 13 weeks. Wrinkle formation, epidermal thickness, skin hydration, and collagen content were assessed. Protein expression related to MAPK/AP-1, TGF-β/Smad2/3, and p53/p21 pathways was analyzed by Western blotting. Results: KP-1 significantly reduced UVB-induced wrinkle area, epidermal and dermal thickening, and transepidermal water loss while restoring collagen density and skin hydration. KP-1 inhibited MMP-1 expression, enhanced COL1A1 levels, suppressed MAPK/AP-1 activation, and activated TGF-β/Smad2/3 signaling. It also balanced p53/p21 expression and restored cyclin D1 and CDK4 levels, thereby preventing UVB-induced senescence. Conclusions: The findings of this research revealed that KP-1 can serve as a promising natural substance for safeguarding the skin from damage and aging caused by UVB exposure. Full article

Ultraviolet B (UVB) radiation triggers DNA damage and immune suppression, establishing conditions favorable for skin carcinogenesis. Previous studies have shown that a downstream adaptor for Toll-like receptors (TLRs), myeloid differentiation primary response 88 (MyD88), plays a role in UVB-induced DNA damage and immunosuppression. However, specific mechanisms for the effects on dendritic cells and T cells remain poorly understood. The objective of this study is to determine the role of MyD88 and TIR-domain-containing adaptor inducing interferon-β (TRIF), another key TLR downstream adaptor, in UVB-induced suppression of dendritic cell activity and T cell function. MyD88−/−, Trif−/−, and wild-type (WT) mice were evaluated for UVB-induced effects on dendritic cell, T cells, and contact hypersensitivity responses in skin. MyD88−/− mice exhibited significant resistance to UVB-induced immune suppression, compared to Trif−/− mice and wild-type controls. The MyD88 deficiency significantly reduced UVB-induced Treg cells that were CD4⁺CD25⁺Foxp3⁺ and produced interleukin (IL)-10. Moreover, it significantly inhibited the UVB-induced suppression of IL-12/IL-23 producing CD11c⁺ dendritic cells. Further experiments confirmed that MyD88 conditional knockout (MyD88fl/flXCD11c.Cre) mice were protected against UVB-induced immune suppression. Dendritic cells from MyD88 genomic or conditional knockout mice were resistant to UVB-induced reduction of major histocompatibility complex (MHC) class II antigens. These findings show that MyD88 plays a key role in UVB-induced immune suppression. The deficiency in the MyD88 gene inhibits UVB-induced suppression of CD11c+ dendritic cell (DC) activity and reduces UVB-induced development of Treg cells. Our studies demonstrate a new mechanism for MyD88-mediated regulation of UVB-induced immune suppression. Full article

UVB radiation penetrates the epidermis and upper dermis, compromising skin barrier function. This activates pro-inflammatory cells, releasing mediators (e.g., histamine, interleukins) that induce edema. UVB also generates excessive reactive oxygen species (ROS), causing oxidative stress in skin cells. Although the mechanisms of UV-induced skin damage have been extensively studied, the development of effective UV-protective drugs remains a significant challenge. Scutellarin, a flavonoid glycoside predominantly isolated from Erigeron breviscapus, has demonstrated diverse bioactivities including anti-inflammatory, antioxidant, and anti-tumor effects. However, its role in UVB-induced skin damage has not been fully explored. Therefore, we established a UVB-induced skin damage model in mice by irradiating the dorsal skin with a dose of 300 mJ/cm² UVB. Through measurements of transepidermal water loss, detection of barrier-related proteins, assessment of inflammatory factors, and evaluation of oxidative stress indicators, we found that scutellarin can maintain barrier integrity, reduce skin edema, suppress inflammatory responses, and decrease oxidative stress. Moreover, RNA sequencing of mice skin revealed that scutellarin can modulate inflammatory responses and maintain extracellular matrix homeostasis to alleviate skin damage. These findings suggest that scutellarin is a natural compound with potential for UV-protective effects on the skin. Full article

Moisturizers are key components of skincare products, and reliable test methods are essential for evaluating their barrier-repairing and hydrating efficacy. However, the viscous and waxy nature of many cosmetic moisturizers limits the applicability of conventional cell-based in vitro assays. In this study, we developed a novel in vitro dry skin model using epidermal sheets from minipig and human cadaver skin—models widely accepted in skin absorption research. To simulate dry skin conditions, various stimuli were applied, including the lipid-extracting solvent tert-butyl methyl ether (MTBE; 100%), 50/50 MTBE/Acetone solution (M/A), the irritant surfactant sodium dodecyl sulfate (SDS; 1%), ultraviolet B (UVB) irradiation (30 mJ/cm²), and tape stripping. Skin barrier disruption and stratum corneum damage were evaluated by assessing epidermal lipid integrity, histological alterations, transepidermal water loss (TEWL), and FITC-dextran permeation. All treatments induced significant dry skin conditions, as evidenced by disrupted lipid architecture, histological damage, and increased TEWL and FITC-dextran flux. Among them, M/A applied for 5 min produced the most consistent and reproducible changes across parameters. This protocol also yielded comparable results in human cadaver skin, supporting its applicability for evaluating the skin barrier-protective effects of cosmetic ingredients. Full article

Ultraviolet B (UVB) radiation is a key factor in the overproduction of melanin in the skin. Melanocytes produce melanin through melanogenesis to protect the skin from UVB radiation-induced damage. However, excessive melanogenesis can lead to hyperpigmentation and increase the risk of malignant melanoma. Tyrosinase is the rate-limiting enzyme in melanogenesis; it catalyzes the oxidation of tyrosine to 3,4-dihydroxy-L-phenylalanine and subsequently to dopaquinone. Thus, inhibiting tyrosinase is a promising strategy for preventing melanogenesis and skin hyperpigmentation. White mulberry (Morus alba L.) is rich in antioxidants, and mulberry fruit extracts have been used as cosmetic skin-lightening agents. However, data on the capacity of mulberry fruit extracts to inhibit tyrosinase under UVB radiation-induced melanogenic conditions remain scarce, especially in an in vivo model. In this study, we evaluated the effects of a mulberry crude extract (MCE) on UVB radiation-induced melanogenesis in B16F10 melanoma cells and zebrafish embryos. The MCE significantly reduced tyrosinase activity and melanogenesis in a dose-dependent manner without inducing cytotoxicity. These effects are likely attributable to the antioxidant constituents of the extract. Our findings highlight the potential of this MCE as an effective tyrosinase inhibitor for the prevention of UVB radiation-induced skin hyperpigmentation. Full article

Skin aging is characterized by compromised epidermal homeostasis and dermo-epidermal junction (DEJ) integrity, resulting in reduced stem cell potential and impaired tissue regeneration. This study investigated the effects of Andrographis paniculata extract (APE) on keratinocyte stem cells (KSCs) and DEJ composition in human skin. Using human skin explants and cell culture models, we demonstrated that APE treatment enhances DEJ composition by increasing Collagen IV and Laminin production while decreasing MMP-9 expression, without altering epidermal structure or differentiation. In the same model, APE preserved stemness potential by upregulating markers related to niche components (collagen XVII and β1-integrin), proliferation (Ki-67 and KRT15), and stem cell capacity (Survivin and LRIG1). In vitro studies revealed that APE selectively stimulated KSC proliferation without affecting transit amplifying cells and promoted Collagen IV and Laminin secretion, particularly in KSCs. Furthermore, in a co-culture model simulating a compromised DEJ (UVB-induced), APE increased Laminin production in KSCs, suggesting a protective effect against photo-damage. These findings indicate that APE enhances DEJ composition and preserves stem cell potential, highlighting its promise as a candidate for skin anti-aging strategies targeting stem cell maintenance and extracellular matrix stability to promote skin regeneration and repair. Full article

Background/Objectives: Ultraviolet B (UVB) radiation contributes significantly to skin aging and skin disorders by promoting oxidative stress, inflammation, and collagen degradation. Natural antioxidants such as theaflavins and thearubigins from Camellia sinensis L. (black tea) have shown photoprotective effects. This study aimed to optimize the extraction of theaflavins and thearubigins from black tea leaves and evaluate the efficacy of the extract against UVB-induced damage using a transfersome-based topical formulation. Methods: Extraction of theaflavins and thearubigins was optimized via response surface methodology (Box-Behnken Design), yielding an extract rich in active polyphenols. This extract was incorporated into transfersomes that were characterized for size, polydispersity, zeta potential, storage stability, and entrapment efficiency. Human dermal fibroblasts (NHDF) were used to assess cytotoxicity, protection against UVB-induced viability loss, collagen degradation, and expression of inflammatory (IL6, COX2, iNOS) and matrix-degrading (MMP1) markers. Cellular uptake of the extract’s bioactive marker compounds was measured via LC-MS/MS. Results: The transfersomes (~60 nm) showed a good stability and a high entrapment efficiency (>85%). The transfersomes significantly protected NHDF cells from UVB-induced cytotoxicity, restored collagen production, and reduced gene expression of MMP1, IL6, COX2, and iNOS. Cellular uptake of key extract’s polyphenols was markedly enhanced by the nanoformulation compared to the free extract. Conclusions: Black tea extract transfersomes effectively prevented UVB-induced oxidative and inflammatory damage in skin fibroblasts. This delivery system enhanced bioavailability of the extract and cellular protection, supporting the use of the optimized extract in cosmeceutical formulations targeting photoaging and UV-induced skin disorders. Full article

Ultraviolet B (UVB) irradiation drives skin photodamage, prompting exploration of natural therapeutics. This study investigated the reparative effects and mechanisms of crude Gastrodia elata polysaccharides (GP) on UVB-induced acute skin damage. GP was extracted from fresh G. elata via water extraction and alcohol precipitation. It is a homogeneous polysaccharide with a weight-average molecular weight of 808.863 kDa, comprising Ara, Glc, Fru, and GalA. Histopathological analysis revealed that topical application of GP on the dorsal skin of mice effectively restored normal physiological structure, suppressing epidermal hyperplasia and collagen degradation. Biochemical assays showed that GP significantly reduced the activities of MPO and MDA following UVB exposure while restoring the enzymatic activities of SOD and GSH, thereby mitigating oxidative stress. Moreover, GP treatment markedly upregulated the anti-inflammatory cytokines TGF-β and IL-10 and downregulated the pro-inflammatory mediators IL-6, IL-1β, and TNF-α, suggesting robust anti-inflammatory effects. Transcriptomics revealed dual-phase mechanisms: Early repair (day 5) involved GP-mediated suppression of hyper inflammation and accelerated necrotic tissue clearance via pathway network modulation. Late phase (day 18) featured enhanced anti-inflammatory, antioxidant, and tissue regeneration processes through energy-sufficient, low-inflammatory pathway networks. Through a synergistic response involving antioxidation, anti-inflammation, promotion of collagen synthesis, and acceleration of skin barrier repair, GP achieves comprehensive repair of UVB-induced acute skin damage. Our findings not only establish GP as a potent natural alternative to synthetic photoprotective agents but also reveal novel pathway network interactions governing polysaccharide-mediated skin regeneration. Full article

Viola philippica (VP), a traditional Chinese medicinal herb widely used for its antibacterial and antioxidant properties, has recently garnered attention for its potential in skin photoprotection. VP was extracted using glycerol (GLY), 1,3-propanediol (PDO), and 1,3-butanediol (BDO) at concentrations of 30%, 60%, and 90% (w/w) to evaluate its antioxidant and UV-protective properties. The total phenolic content (TPC) and total flavonoid content (TFC) of the nine extracts ranged from 34.73 to 71.45 mg GAEs/g and from 26.68 to 46.68 mg REs/g, respectively, with the highest TPC observed in 90% PDO and the highest TFC in 60% GLY. Antioxidant assays revealed IC₅₀ values of 0.49–1.26 mg/mL (DPPH), 0.10–0.19 mg/mL (ABTS), and 1.58–460.95 mg/mL (OH). Notably, the 60% GLY, 30% PDO, and 90% PDO extracts demonstrated notable protective effects against UVB-induced cell damage, reducing intracellular ROS levels and preventing DNA damage. RNA-seq analysis revealed that the protective effects were associated with the modulation of key molecular pathways, including neutrophil extracellular trap formation and TNF, IL-17, and HIF-1 signaling. These findings suggest that Viola philippica polyol extracts, particularly those using 60% GLY, 30% PDO, and 90% PDO, have promising potential for skin photoprotection and could be utilized as natural antioxidants in cosmetic formulations. Full article

Ultraviolet B (UVB), a component of solar ultraviolet light, is a major contributor to skin photodamage. UVB exposure primarily affects the epidermis, which leads to wrinkle formation, loss of skin elasticity, oxidative stress, and inflammation. Prolonged or intense UVB exposure can increase the risk of skin cancer. Collagen peptides are known as functional foods that improve skin dryness and wound healing. In this study, we aimed to investigate the protective and ameliorative effects of a low-molecular-weight collagen peptide (LMWCP) with a high absorption rate and photodamage. In vitro analysis using human dermal fibroblasts (HDFs) demonstrated that LMWCP promoted skin protection by increasing procollagen type I production, enhancing cell proliferation and migration, and inhibiting MMP-1 activity. Furthermore, LMWCP intake was indicated by improved skin hydration, reduced trans-epidermal water loss (TEWL), and changes in the clinical parameters, including skin elasticity, erythema, and scaling scores in UVB-exposed hairless mice. In the UVB-damaged tissues, an increase in skin elasticity-related enzymes was observed along with a decrease in aging-related and pro-inflammatory gene expression. Histological analysis revealed an increase in collagen content and restoration of dermal thickness. These findings suggested that LMWCP has significant benefits in preventing and improving UVB-induced skin damage. Full article

Skin damage and premature aging are predominantly driven by UV radiation through several mechanisms. The most common of these are by reactive oxygen species (ROS) generation, upregulation of matrix metalloproteinases (MMPs), and weakened antioxidant defenses. Moringa oleifera is a nutritionally valuable plant with diverse biological activities. This study optimized ethanol concentrations coupled with ultrasonic-assisted extraction to maximize the yield and efficacy of M. oleifera leaf extract (MOLE). We also elucidated the underlying mechanisms of MOLE in protecting against photooxidative damage and skin aging from UVB exposure in HaCaT keratinocytes. Extraction with 50% ethanol produced the highest total phenolic and flavonoid contents, aligning with the greatest antioxidant activity by ABTS and FRAP assays. MOLE showed no significant cytotoxicity up to 1000 µg/mL in the MTT assay. MOLE protected cells from detrimental UVB radiation by scavenging ROS; reducing cell damage and death; enhancing gene expression of superoxide dismutase (SOD-1), glutathione peroxidase (GPx), and catalase (CAT); and improving SOD activity. UVB exposure elevated MMP-1, MMP-3, and MMP-9 expression and decreased collagen type I (col-1) and elastin (ELN) expression, while these effects were ameliorated by MOLE. Our findings suggest that MOLE protected against UVB-induced photooxidative damage and premature aging in the HaCaT keratinocytes. Full article

Background/Objectives: Actinic keratosis (AK) occurs on sun-damaged skin and is considered a precursor to squamous cell carcinoma (SCC). Photodynamic therapy (PDT), using 5-aminolevulinic acid (ALA) and red light, is a common treatment for AK. However, its clinical efficacy for invasive tumors such as SCC is limited by the poor penetration and distribution of the photosensitizer. Cold atmospheric plasma (CAP), a partially ionized gas, increases skin permeability and exhibits anti-cancer properties through the generation of reactive oxygen species (ROS). In a previous study, CAP showed promising synergistic effects when combined with ALA-PDT for the treatment of SCC cells in vitro. The present study investigated the effects of combining CAP with ALA-PDT on cutaneous AK and SCC induced by ultraviolet B (UV-B) irradiation in SKH1 hairless mice. Methods: We compared various application sequences (CAP-ALA–red light, ALA–red light–CAP, and ALA-CAP–red light) against conventional ALA-PDT using visual, histological, and molecular assessments of the affected skin. Results: The results demonstrated that combined treatments strongly inhibited the growth of UV-B-induced skin lesions. TUNEL staining revealed increased apoptosis following both single and combined therapies, while Ki-67 staining indicated reduced keratinocyte proliferation and diminished DNA damage in treated areas. mRNA expression analysis showed the upregulation of apoptosis-related genes (p16^INK4a, p21^CIP1) alongside enhanced anti-tumor immune responses (IL-6, IL-8) in the affected tissue samples. Notably, the combined treatment enhances the therapeutic effect, whereas the sequence of application does not seem to be relevant for therapeutic efficacy in vivo. Conclusions: Overall, these results suggest that CAP may enhance the anti-tumor effect of conventional ALA-PDT, supporting previous findings on SCC cells. Full article

Prolonged exposure to ultraviolet (UV) radiations represents a significant risk factor and may lead to various skin disorders, premature aging, and an increased susceptibility to skin cancers. Recently, probiotics have emerged as promising candidates for fortifying the skin’s natural defences through their diverse mechanisms. The aim of the present work was exploring the potential of five heat-treated probiotics (Skinbac^TM, Probiotical Research S.r.l., Novara, Italy), as protective agents against UVA and UVB damages on human keratinocyte line (HaCaT) and human skin 3D model (Phenion^® Full-Thickness Skin Model, Henkel AG & Co. KGaA, Dusseldorf, Germany). The protective role toward artificially induced oxidative stress was evaluated by determining the residual viability after UV exposure and analyzing gene expression of markers involved in apoptosis (Tumor protein 53), inflammation/immunosuppression (Interleukin 6), oxidative stress (oxidative stress response enzyme heme oxygenase 1), investigated using quantitative real-time PCR. Additionally, we examined the protective effects of these strains, testing them on Normal Human Epidermal Keratinocytes (NHEK) irradiated with UVC, specifically, evaluating the expression of tight junction proteins, including claudin 1, claudin 4, and occludin, by ELISA. The tested heat-treated probiotics effectively protected from UVA, UVB, and UVC damage on all end points analyzed, revealing their capacity to enhance barrier protection in cases of damage and their potential for innovative skincare strategies centered around probiotic-based formulations for enhanced protection against UV-induced skin damage. Full article

Ultraviolet (UV) radiation is a predominant cause of skin damage, with UVB leading to more severe harm compared to UVA. Lycium barbarum L. (L. barbarum) is known for its high carotenoid content and has shown great potential in mitigating UVB-induced skin damage. This study investigated the protective effect and mechanism of zeaxanthin from L. barbarum on UVB-damaged skin in BALB/c mice. The results demonstrated that zeaxanthin effectively alleviated the UVB-injured appearance of mouse skin. Histological analyses revealed a reduction in epidermal thickness by 30% and 61% with low and high doses of zeaxanthin, respectively, compared to the model group. Zeaxanthin also inhibited the degeneration of elastic and collagen fibers. Further investigations indicated that the protective mechanism of zeaxanthin was not involved with inflammation suppression. Instead, it activated nuclear factor erythroid 2-related factor 2 (Nrf2) to approximately 3 times the level of the model group, significantly promoting the expression of various antioxidant enzymes and enhancing the total antioxidant capacity of skin tissue, subsequently reducing oxidative stress. Zeaxanthin also downregulated the expression of matrix metalloproteinases, reducing collagen degradation by 35% compared to the model group, which led to improved skin tissue structure and protection against UVB-induced photodamage. These findings provided a theoretical basis for the advanced development and high-value utilization of carotenoids in L. barbarum. Full article

Lysine carboxymethyl cysteinate (LCC) is a synthetic substance obtained via lysine salification of S-carboxymethyl-cysteine. LCC has emerged as a promising glutathione (GSH) precursor. In this study, we sought to determine whether LCC could boost GSH levels and protect skin against oxidative stress. Experiments utilizing primary human keratinocytes and skin tissue samples revealed that LCC significantly increased endogenous GSH levels. LCC was able to pass through the stratum corneum and reach deep into the epidermis, where it enhanced the production of key metabolites involved in GSH biosynthesis. Then, the efficacy of LCC on skin protection was explored. LCC demonstrated protective effects by shielding keratinocytes from blue-light-induced oxidative stress and preventing ultraviolet B (UVB)-induced barrier disruption and pigmentation in a pigmented living skin equivalent (pLSE) model. In addition to its antioxidant properties, LCC also reduced the production of inflammatory mediators. Together, these findings underscore the multifaceted role of LCC in bolstering the natural antioxidant defenses of skin and preventing the accumulation of irreversible damage from the environment, thereby positioning it as a promising candidate for advancing skin health. Full article