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Skin aging is influenced by both intrinsic and extrinsic factors, particularly UV radiation, and is characterized by an accumulation of senescent cells. Remarkably, exposure to UV can trigger senescence in different skin cell types, including dermal fibroblasts. However, the molecular mechanisms underlying UV‐induced senescence and the impact of the related senescence‐associated secretory phenotype (SASP) on the homeostasis of the overlying epidermis remain poorly understood. Here, we identified that both chronological aging and photoaging induce the unfolded protein response (UPR) in human dermal samples. We demonstrated that silencing ATF6α disrupts the establishment of the UVB‐induced senescent phenotype by preventing the onset of several senescent biomarkers and alters the composition of the SASP, consequently affecting its impact on the increased proliferation of keratinocytes embedded in reconstructed human epidermis. Moreover, we found that ATF6α partially mediates IL8 expression involved in the hyperproliferation of cultured keratinocytes. Together, our findings highlight the importance of the ATF6α/IL8 axis in regulating the homeostasis of neighboring cells during skin photoaging, thus suggesting ATF6α as a potentially promising target for senotherapeutic interventions. UVB exposure can trigger senescence in dermal fibroblasts. We show that silencing ATF6α disrupts the establishment of the UVB‐induced senescent phenotype by preventing the onset of several senescent biomarkers and altering the composition of the SASP, consequently affecting its impact on the skin microenvironment.

Background Although the role of platelet‐rich plasma (PRP) in ultraviolet light B (UVB)‐induced photoaging has been confirmed in many studies, the specific mechanism is still not clear. Therefore, we attempted to investigate the effect and mechanism of PRP on UVB‐induced human keratinocyte (HaCaT cells) apoptosis. Methods HaCaT cells were collected to construct UVB‐induced photoaging models. Then, the cells were divided into Sham group, 5% PRP group, UVB group, and UVB + 5% PRP group. Next, MTT assay was used to detect the level of cell proliferation; flow cytometry to check the level of apoptosis; ELISA to determine the TNF‐α, IL‐18, IL‐6, and IL‐1β levels in the supernatant; and Western blot to test Bax, Bcl‐2, cytochrome c (Cyt.c), GRP78, CHOP, and ATF4 protein expression levels. Results Briefly, 5% PRP intervention could relieve the inhibition of UVB on HaCaT cell proliferation, inhibit the promotion of UVB to cell apoptosis, up‐regulate UVB‐induced Bcl‐2 protein expression, and decrease Bax and Cyt.c protein level. In addition, 5% PRP significantly down‐regulated the inflammatory factor levels of TNF‐α, IL‐18, IL‐6, and IL‐1βin UVB‐induced cells and reduced the inflammatory response. Moreover, 5% PRP also greatly reduced the protein expression levels of GRP78, CHOP, and ATF4 in UVB‐induced cells and alleviated endoplasmic reticulum (ER) stress. Conclusion PRP may protect HaCaT cells from UVB‐induced apoptosis by alleviating inflammatory response and ER stress.

Ultraviolet (UV) radiation exposure to the cornea can lead to photokeratitis, disrupting tear film homeostasis and increasing the risk of dry eye disease (DED). While Cordyceps cicadae mycelium extracts (CCME) have been reported to benefit ocular diseases, their potential to alleviate UVB‐induced photokeratitis remains unexplored. This study investigated the CCME's protective effects against UVB‐induced corneal damage. ICR mice were randomly assigned to three groups: a control group, a UVB‐exposed group with vehicle treatment (UVB group), and a UVB‐exposed group treated with CCME (CCME group). Tear volume (TV), tear break‐up time (TBUT), ocular surface integrity, conjunctival goblet cell density, and inflammatory markers were evaluated. The results demonstrated that CCME intake significantly improved TV and TBUT, while reducing oxidative stress and inflammatory markers (p63 + , PCNA, NF‐κB, and COX‐2). Notably, CCME treatment helped to preserve goblet cells and maintain Muc5Ac expression therein, with concomitant suppression on lipid peroxidation (as indicated by MDA and 4‐HNE reduction) in the meibomian glands, suggesting its role in stabilizing tear film composition. This study advances the field by introducing CCME as a potential therapeutic agent for photokeratitis, offering a natural, oral treatment alternative with anti‐inflammatory and antioxidative properties. CCME could help prevent progression to chronic DED and other ocular surface disorders by mitigating corneal inflammation and preserving tear film components. Given the elevated prevalence of UV‐induced ocular damage due to environmental changes, these findings provide a foundation for developing CCME‐based interventions in ophthalmology, bridging traditional medicine with modern therapeutic interventions. Cordyceps cicadae mycelium extracts (CCME) have been reported to exert beneficial effects on ocular diseases. TV, TBUT, and cornea surface indexes were improved with oral CCME intake. Immunohistochemical assays showed that p63 + , PCNA, NF‐κB and COX‐2 expressions decreased in the CCME group than that of the UVB group. The corneas of those treated with CCME also showed maintained conjunctival goblet cells density and normal Muc5Ac expression after UVB damage. Lipid peroxidation biomarkers MDA and 4‐HNE were not detected in the meibomian glands in the CCME group.

Excessive exposure to ultraviolet B (UVB) radiation induces oxidative stress and inflammatory responses, accelerating the senescence process of skin cells. Vorinostat (SAHA), a histone deacetylase inhibitor (HDACi), is typically administered to patients with peripheral T-cell lymphoma, cutaneous T-cell lymphoma, or multiple myeloma. However, its effect on UVB-induced skin photoaging remains unclear. In this study, we used UVB to induce senescence in human immortalized keratinocyte cell line (HaCaT cells) and skin photoaging in Balb/c mice to investigate the potential of SAHA in mitigating photoaging. First, we established a UVB-induced photoaging model in HaCaT cells. We observed that UVB exposure significantly upregulated the activity of senescence-associated β-galactosidase, p16, p21, IL-1β, IL-6, and matrix metalloproteinases [collagenase (MMP-1), matrix metalloproteinase-3 (MMP-3), and gelatinase (MMP-9)]. Supplementation with SAHA effectively alleviated cellular senescence in HaCaT cells. Next, we used UVB to induce photoaging in Balb/c mouse skin. The study demonstrated that UVB markedly caused skin senescence in Balb/c mice, while SAHA effectively mitigated the changes induced by UVB irradiation. Mechanistically, we found that UVB activated the mammalian target of rapamycin (mTOR) and nuclear factor-κB (NF-κB) signaling pathways, whereas SAHA inhibited the upregulation of both mTOR and NF-κB. In summary, these findings suggest that SAHA may protect against UVB-induced cellular senescence and skin photoaging by inhibiting the mTOR and NF-κB signaling pathways. Therefore, SAHA could be a potential anti-senescence agent for mitigating skin photoaging.

Skin aging is driven by oxidative stress, extracellular matrix degradation, and ultraviolet-B (UVB)-induced cellular injury. Plant-derived bioactives with multi-targeted protective actions offer promising avenues for cosmeceutical development. This study assessed ethanolic leaf extracts of Vitex trifolia, an Indonesian medicinal plant traditionally used for skin disorders. Phytochemical analysis showed a total phenolic content of 78.52 ± 0.01 mg GAE/g and total flavonoid content of 1.99 ± 0.02 mg QE/g. LC–HRMS profiling identified major flavonoid and phenolic acid derivatives. Antioxidant assays demonstrated strong radical-scavenging and reducing activities, with IC50 values of 63.47 ± 0.24 (DPPH) and 70.13 ± 1.28 μg/mL (ABTS) and a Ferric Reducing Antioxidant Power (FRAP) value of 36.3 ± 0.18 FeSO4 eq/100 g. Enzymatic studies confirmed potent collagenase inhibition (IC50 = 27.94 ± 3.20 μg/mL) and moderate elastase inhibition, supported by molecular docking analysis. In HaCaT keratinocytes, the extract remained non-cytotoxic up to 100 μg/mL and exerted cytoprotective activity against UVB-induced damage at 12.5–50 μg/mL. The extract also downregulated UVB-induced matrix metalloproteinase-1 (MMP-1) and matrix metalloproteinase-9 (MMP-9) expression up to 42% and 69%, respectively, outperforming ascorbic acid. These findings highlight V. trifolia as a multifunctional natural candidate for anti-photoaging cosmeceutical applications over single-compound antioxidants, as demonstrated by its combined antioxidant, enzyme-inhibitory, cytoprotective, and MMP-modulating activities, as well as a wider cell safety profile.

Retinyl palmitate (RP) is a vitamin A derivative that has been widely used in anti-aging and skin treatment. The aim of this study is to investigate the effect of RP on UVB (Ultraviolet radiation B) induced photoaging and its potential mechanism. Immunofluorescence assay demonstrates that RP can reduce collagen degradation in skin cells by UVB radiation and reduce apoptosis of skin cells. Cell migration assay reveals that RP can increase cell migration rate, helping to repair skin damage and restore cell viability. Immunohistochemical assays indicate that RP can significantly reduce the expression of IL-6, IL-1β, TNF-α induced by UVB radiation. Moreover, metabolomics and transcriptomics results suggest that RP regulates several metabolic pathways and gene expression, particularly in inflammatory signaling pathways, collagen synthesis and apoptosis, exhibiting significant regulatory effects. Furthermore, network pharmacological analysis predicts that RP may affect UVB-induced photoaging by regulating multiple key proteins and signaling pathways. Overall, this study demonstrates that RP has significant anti-photoaging ability, acting through several pathways including inhibition of inflammatory response, promotion of collagen synthesis and inhibition of apoptosis. These results provide a scientific basis for the application of RP in skin anti-photoaging and therapy, enabling the potential usage of RP to skin care products.

Centella asiatica exhibits antioxidant, anti-inflammatory, and dermal-regenerative activities, yet the in vivo efficacy of an orally administered, dose-standardized extract against ultraviolet B (UVB)-induced photoaging has not been fully elucidated. This study investigated the protective effects of a chemically standardized C. asiatica extract (sCAE; 70 mg/g asiaticoside) in UVB-irradiated Skh:HR-1 hairless mice. Animals received oral sCAE (40 or 80 mg/kg/day) for eight weeks during repeated UVB exposure. Comprehensive assessments—including skin biophysical measurements, histological analysis, ELISA, and gene expression profiling—were performed to characterize dose-dependent responses. sCAE significantly reduced wrinkle formation, transepidermal water loss, malondialdehyde accumulation, and pro-inflammatory cytokines, while enhancing skin hydration, elasticity, antioxidant enzyme activities, and collagen expression. It also restored hyaluronic acid, ceramide, and their biosynthetic genes, and suppressed matrix metalloproteinase-1 and -9. Notably, the higher dose (80 mg/kg) consistently shifted key parameters toward normal levels, demonstrating a clear dose–response effect. These findings provide the first integrative in vivo evidence that orally administered, asiaticoside-standardized C. asiatica extract mitigates UVB-induced photoaging by concurrently improving barrier lipids, extracellular matrix integrity, inflammation, and oxidative stress, supporting its potential as a nutricosmetic agent for skin health.

Aloin, an anthraquinone compound, is naturally abundant in the Aloe . This study comprehensively investigates the photoprotective effects of aloin against UVB-induced damage in HaCaT cells, elucidating its antioxidant capacity and its role in preventing cellular apoptosis. Aloin demonstrated significant antioxidant activity in ABTS and DPPH assays, with a dose-dependent reduction in intracellular reactive oxygen species levels as evidenced by fluorescence analysis. Western blot analysis revealed that aloin inhibited the phosphorylation of both p38 and JNK, with a more pronounced effect on p38. This was further supported by IC50 values, indicating a higher inhibitory potency of aloin against p38 compared to JNK. Assessments using MTT, Hoechst, Calcein/PI staining, and flow cytometry collectively verified that aloin effectively mitigated UVB-induced apoptosis in cells. Proteomic analysis showed that aloin modulated the expression of proteins involved in critical signaling pathways, including PI3K-Akt, p53, TGF-β and pathways in cancer, promoting cell survival. Aloin upregulated proteins associated with cell cycle regulation and antioxidant responses, such as CCND3, GSTM4, GNA12, SKIL, YWHAZ, and PKN3 while downregulating pro-apoptotic protein FOXO3. These findings highlight aloin’s potential as a therapeutic agent for UVB-induced skin damage by effectively modulating cellular stress responses.

Natural products used in the treatment of acne vulgaris may be promising alternative therapies with fewer side effects and without antibiotic resistance. The objective of this study was to formulate creams containing Spirulina (Arthrospira) platensis to be used in acne therapy. Spirulina platensis belongs to the group of micro algae and contains valuable active ingredients. The aim was to select the appropriate nonionic surfactants for the formulations in order to enhance the diffusion of the active substance and to certify the antioxidant and antibacterial activity of Spirulina platensis-containing creams. Lyophilized Spirulina platensis powder (SPP) was dissolved in Transcutol HP (TC) and different types of nonionic surfactants (Polysorbate 60 (P60), Cremophor A6:A25 (CR) (1:1), Tefose 63 (TFS), or sucrose ester SP 70 (SP70)) were incorporated in creams as emulsifying agents. The drug release was evaluated by the Franz diffusion method and biocompatibility was tested on HaCaT cells. In vitro antioxidant assays were also performed, and superoxide dismutase (SOD) and 2,2-diphenyl-1-picrylhydrazyl (DPPH) assays were executed. Antimicrobial activities of the selected compositions were checked against Staphylococcus aureus (S. aureus) and Cutibacteriumacnes (C. acnes) (formerly Propionibacterium acnes) with the broth microdilution method. Formulations containing SP 70 surfactant with TC showed the most favorable dissolution profiles and were found to be nontoxic. This composition also showed significant increase in free radical scavenger activity compared to the blank sample and the highest SOD enzyme activity was also detected after treatment with the cream samples. In antibacterial studies, significant differences were observed between the treated and control groups after an incubation time of 6 h.

Prinsepia utilis seed oil (PUSO) is a natural medication obtained from Prinsepia utilis Rogle seed, which has been used for the treatment of skin diseases. The study aims to prepare ethosomes with high drug loading as a water-soluble transdermal vehicle to enhance the transdermal delivery of PUSO. PUSO-loaded ethosomes (PEs) were prepared using a cold method, and optimized by an orthogonal experimental design with entrapment efficiency (EE) as the dependent variable. The PEs prepared with the optimized formulation showed good stability, with a spherical shape under transmission electron microscopy (TEM), average particle size of 39.12 ± 0.85 nm, PDI of 0.270 ± 0.01, zeta potential of -11.3 ± 0.24 mV, and EE of 95.93 ± 0.43%. PEs significantly increased the skin deposition of PUSO compared to the PUSO suspension ( P < 0.001). Moreover, the optimum formula showed significant ameliorative effects on ultraviolet B (UVB) irradiation-associated macroscopic and histopathological changes in mice skin. Therefore, PEs represent a promising therapeutic approach for the treatment of UVB-induced skin inflammation, with the potential for industrialization. Graphical Abstract