Anti-photoaging Effects Research Articles

Mitigating Glycation and Oxidative Stress in Aesthetic Medicine: Hyaluronic Acid and Trehalose Synergy for Anti-AGEs Action in Skin Aging Treatment.

This comprehensive review explores the pivotal roles of glycation and oxidative stress in the aging process of the skin, emphasizing their targeted therapeutic applications in aesthetic and regenerative medicine, as well as anti-aging interventions. Glycation, a biochemical process involving the non-enzymatic attachment of sugars to proteins, lipids, or nucleic acids, culminates in the formation of Advanced Glycation End products (AGEs). These AGEs are significant contributors to aging and various chronic ailments, triggering oxidative stress and inflammatory pathways, thereby manifesting as wrinkles, diminished skin elasticity, and other age-related dermal alterations. A central focus of this review is the synergistic interplay between Hyaluronic Acid (HA) and Trehalose in combating these aging mechanisms. HA, renowned for its anti-inflammatory and antioxidative properties, assumes a pivotal role in modulating Reactive Oxygen Species (ROS) levels and safeguarding against oxidative damage. Concurrently, trehalose targets glycation and oxidative stress, exhibiting promising outcomes in augmenting skin health, providing Ultraviolet B (UVB) photoprotection, and manifesting notable anti-photoaging effects. The combined administration of HA and trehalose not only addresses existing skin damage but also confers preventive and reparative benefits, particularly in stabilizing HA and mitigating glycation-induced stress. Their synergistic action significantly enhances skin quality and mitigates inflammation. The implications of these findings are profound for the future of anti-aging therapeutics in aesthetic medicine, suggesting that the integration of HA and trehalose holds promise for revolutionary advancements in preserving skin vitality and health. Moreover this paper underscores the imperative for continued research into the combined efficacy of these compounds, advocating for innovative therapeutic modalities in aesthetic medicine and enhanced strategies for combating aging, glycation, and oxidative stress.

Anti-Photoaging Effects of Antioxidant Peptide from Seahorse (Hippocampus abdominalis) in In Vivo and In Vitro Models.

Overexposure to ultraviolet (UV) radiation can lead to photoaging, which contributes to skin damage. The objective of this study was to evaluate the effects of an antioxidant peptide (SHP2) purified from seahorse (Hippocampus abdominalis) alcalase hydrolysate on UVB-irradiated skin damage in human keratinocyte (HaCaT) and human dermal fibroblast (HDF) cells and a zebrafish model. The data revealed that SHP2 significantly enhanced cell viability by attenuating apoptosis through the reduction of intracellular reactive oxygen species (ROS) levels in UVB-stimulated HaCaT cells. Moreover, SHP2 effectively inhibited ROS, improved collagen synthesis, and suppressed the secretion of matrix metalloproteinases (MMPs) in UVB-irradiated HDF cells. SHP2 restored the protein levels of HO-1, Nrf2, and SOD, while decreasing Keap1 expression in UVB-treated HDF, indicating stimulation of the Keap1/Nrf2/HO-1 signaling pathway. Furthermore, an in vivo study conducted in zebrafish confirmed that SHP2 inhibited photoaging by reducing cell death through the suppression of ROS generation and lipid peroxidation. Particularly, 200 µg/mL of SHP2 exerted a remarkable anti-photoaging effect on both in vitro and in vivo models. These results demonstrate that SHP2 possesses antioxidant properties and regulates skin photoaging activities, suggesting that SHP2 may have the potential for use in the development of cosmetic products.

Galloyl–RGD, Derived from a Fusion of Phytochemicals and RGD Peptides, Regulates Photoaging via the MAPK/AP-1 Mechanism in Human Dermal Fibroblasts

Galloyl–RGD is a novel compound that combines gallic acid with RGD peptides (arginine, glycine, and asparaginic acid) to overcome the problems associated with gallic acid, such as instability at high temperatures and low solubility. In this study, we investigated the effects and molecular mechanisms of action of galloyl–RGD on UVB-induced skin photoaging in human dermal fibroblasts-neonatal (HDF-n). Galloyl–RGD increased collagen synthesis by inhibiting UVB-induced MMP-1 via inhibiting extracellular signal-regulated kinase and Jun N-terminal kinase and their downstream mitogen-activated protein kinase signaling, which are known to be representative photoaging mechanisms. The results of this study will be helpful for understanding the anti-photoaging effect and mechanism of galloyl–RGD and its future applications in the cosmetic and pharmaceutical industries.

Protective Effects of Sesame Glycoproteins on Ultraviolet-Induced Skin Aging: In Vitro and In Vivo Studies.

Ultraviolet (UV) radiation is a primary factor in skin photoaging, leading to wrinkles, reduced elasticity, and pigmentation changes due to damage to cellular DNA, proteins, and lipids. Glycoproteins from sesame cake (SPE) have potential protective effects against UV-induced skin aging. This study investigated the anti-photoaging effects of SPE on UV-induced damage in human keratinocyte HaCaT cells and SKH-1 hairless mice. SPE was evaluated for its ability to mitigate UV-induced damage in HaCaT cells by assessing MMP-1 protein and mRNA expression levels, as well as the activity of transcription factors AP-1 and NF-κB. The phosphorylation of AKT and MAPK pathways was also analyzed. In vivo, SKH-1 hairless mice were exposed to UV radiation, and the effects of SPE on wrinkle formation and skin structure were assessed by measuring wrinkle length, area, and volume. SPE significantly inhibited UV-induced MMP-1 protein and mRNA expression in HaCaT cells, indicating suppression of AP-1 and NF-κB transcription factors involved in MMP-1 production. Additionally, SPE reduced UV-induced phosphorylation of AKT and MAPK pathways. In SKH-1 hairless mice, SPE treatment led to significant reductions in wrinkle length, area, and volume, preserving skin structure in UV-exposed mice. The findings demonstrate that SPE has protective effects against UV-induced photoaging by inhibiting key molecular pathways associated with skin aging. SPE shows promise as a natural anti-photoaging agent, providing a foundation for future skincare product development. Further studies are warranted to explore the molecular mechanisms in detail and to validate these effects through clinical trials.

α-Arbutin ameliorates UVA-induced photoaging through regulation of the SIRT3/PGC-1α pathway.

Owing to its tyrosinase inhibitory activity, α-arbutin has been added to several skin care products as a skin-lightening agent. However, the protective effect of α-arbutin against ultraviolet A (UVA)-induced photoaging has not been well investigated. The present study was designed to investigate the photoprotective effect and mechanism of α-arbutin against UVA-induced photoaging. In vitro experiments, HaCaT cells were treated with UVA at a dose of 3J/cm2 to evaluate the anti-photoaging effect of α-arbutin. α-Arbutin was found to exhibit a strong antioxidant effect by increasing glutathione (GSH) level and inhibiting reactive oxygen species (ROS) production. Meanwhile, α-arbutin markedly improved the expression of sirtuin 3 (SIRT3) and peroxisome proliferator-activated receptor γ coactivator 1 α (PGC-1α) proteins, initiating downstream signaling to increase mitochondrial membrane potential and mediate mitochondrial biogenesis, and improve mitochondrial structure significantly. In vivo analysis, the mice with shaved back hair were irradiated with a cumulative UVA dose of 10J/cm2 and a cumulative ultraviolet B (UVB) dose of 0.63J/cm2. The animal experiments demonstrated that α-arbutin increased the expression of SIRT3 and PGC-1α proteins in the back skin of mice, thereby reducing UV-induced skin damage. In conclusion, α-arbutin protects HaCaT cells and mice from UVA damage by regulating SIRT3/PGC-1α signaling pathway.

A cutting-edge atomization-based methodology for enhancing formulation ability to resist photoaging

BackgroundSkin photoaging mainly occurs in exposed skin irradiated by ultraviolet rays from the sunlight. When exposed to ultraviolet rays, the skin will undergo certain changes to avoid damage. The inflammatory factors produced by light stimulation will induce melanocytes to produce more melanin, leading to the skin shows a rough, dark, dry, loose, and leathery appearance. In particular, when the skin is exposed to external damage and then received the damage of sunlight, such as after an aesthetic medicine treatment, it is more likely to produce post-inflammatory hyperpigmentation (PIH). However, there is a lack of a non-invasive and efficient solution. ObjectiveThe purpose of this study is to verify a new skincare method to resist photoaging. The essence itself has a very good effect in resisting photodamage, when it through atomized to skin, it showcases a non-invasive but better-result approach to skin care. Materials and MethodsThis study assessed anti-photoaging effects through in vitro (antioxidant, UVB protection, ROS tests) and human trials. In vitro results indicate the essence's efficacy. A randomized trial with 60 women (20-45 years, sensitive skin) compared atomized essence vs. smear control. After 28 days, atomized essence improved skin hydration, gloss, reduced redness, TiVi, TEWL, and UV protection. A 7-day test with Moyal Luminous Serum and Atomizer showed this skincare combo effectively prevents photodamage. ResultsThrough in vitro and human experiments, we have verified that the self-developed essence itself has a very good effect of anti-photoaging. Through further comparison of human efficacy tests, we found that with the support of an atomizer, the anti-photoaging effect of the essence has been improved. ConclusionEssence through atomization to resists photoaging, improves skin moisture, gloss, UV protection and reduces redness. Its non-invasive delivery ensures efficacy and user-friendliness.

Preventive effects of dietary fucoxanthin on ultraviolet A induced photoaging in hairless mice.

Repeated exposure to ultraviolet A (UVA) irradiation, which can penetrate the epidermis and reach the dermis, is one of the major causes of skin photoaging. Photoaged skin is characterized clinically by generalized wrinkling, a dry and loose appearance, and seborrheic keratoses, along with skin barrier dysfunction. Fucoxanthin, a xanthophyll carotenoid with a specific allenic bond and 5,6-monoepoxide in its structure, has been found to serve various functions as a food supplement. In the present study, the protective effects of orally administered fucoxanthin at relatively low concentrations (0.001% and 0.01%) against UVA induced photoaging were evaluated in vivo using hairless mice. Oral supplementation of 0.001% fucoxanthin was sufficient for its metabolites to accumulate in the skin, thereby inhibiting pathological changes induced by UVA irradiation, including impaired skin barrier function and accelerated wrinkle formation. Analysis of gene expression revealed that dietary fucoxanthin exerted antiphotoaging effects, possibly by modulating natural moisturizing factor (NMF) synthesis, desquamation, and ceramide composition in the epidermis, and by inhibiting the UVA induced degradation of collagen fibers and inflammation in the dermis. Taken together, our data indicate the potential application of dietary fucoxanthin as a novel ingredient in nutricosmetics for skin care against photoaging. © 2024 Society of Chemical Industry.

Regulatory Mechanisms of Natural Active Ingredients and Compounds on Keratinocytes and Fibroblasts in Mitigating Skin Photoaging.

The mechanism underlying skin photoaging remains elusive because of the intricate cellular and molecular changes that contribute to this phenomenon, which have yet to be elucidated. In photoaging, the roles of keratinocytes and fibroblasts are vital for maintaining skin structure and elasticity. But these cells can get photo-induced damage during photoaging, causing skin morphological changes. Recently, the function of natural active ingredients in treating and preventing photoaging has drawn more attention, with researches often focusing on keratinocytes and fibroblasts. We searched for studies published from 2007 to January 2024 in the Web of Science, PubMed, and ScienceDirect databases through the following keywords: natural plant, natural plant products or phytochemicals, traditional Chinese Medicine or Chinese herbal, plant extracts, solar skin aging, skin photoaging, and skin wrinkling. This review conducted the accordance of Preferred Reporting Items for Systematic Reviews and Meta-Analysis guidelines. In total, 87 researches were included in this review (Figure 1). In keratinocytes, natural compounds may primarily regulate signal pathways such as the NF-κB, MAPK, PI3K/AKT, and Nrf2/ARE pathways, reducing inflammation and cellular damage, thus slowing skin photoaging. Additionally, in fibroblasts, natural active ingredients primarily promote the TGF-β pathway, inhibit MMPs activity, and enhance collagen synthesis while potentially modulating the mTOR pathway, thereby protecting the dermal collagen network and reducing wrinkle formation. Several trials showed that natural compounds that regulate keratinocytes and fibroblasts responses have significant and safe therapeutic effects. The demand for natural product-based ingredients in sunscreen formulations is rising. Natural compounds show promising anti-photoaging effects by targeting cellular pathways in keratinocytes and fibroblasts, providing potential therapeutic strategies. However, comprehensive clinical studies are needed to verify their efficacy and safety in mitigating photoaging, which should use advanced pharmacological methods to uncover the complex anti-photoaging mechanisms of natural compounds.

Structural characteristics and anti-photoaging effect of Pyracantha fortuneana fruit polysaccharides in vitro and in vivo

Pyracantha fortuneana is a cultivated pant extensively cultivated worldwide for its ornamental value and ecological benefits. In this study, a polysaccharide with anti-photoaging activity was extracted and purified from P. fortuneana fruit (PPFP). The structural constitution of PPFP was elucidated by molecular weight determination, FT-IR, monosaccharide composition analysis, smith degradation, methylation, and NMR spectroscopy. The results revealed that PPFP is a macromolecular polysaccharide with a weight-average molecular weight of 70,895 Da. The PPFP is predominantly characterized by →3,6)-β-Galp-(1→, →5,3)-α-Araf-(1 → and →4,2)-α-Xylp-(1→, →4)-β-Galp-(1 → and →4)-β-GalpA-(1 → glycosidic linkages, with t-α-Araf-(1 → and t-α-Glcp-(1 → terminal units. The anti-photoaging activity and potential mechanism of action of PPFP was investigated in vitro and in vivo. Results showed that PPFP exerted anti-photoaging effect on UVB-damaged HaCaT cells by ameliorating cell apoptosis, regulating the mitochondrial membrane potential and oxidative stress level, alleviating the phosphorylation level of the proteins in MAPK pathways, and repairing the expression of tight junction proteins. Moreover, PPFP enhanced the lifespan and diminished the oxidative stress in UVB-injured Caenorhabditis elegans. Collectively, this study comprehensively elucidates the anti-photodamaging potential of P. fortuneana fruit polysaccharide and offers a novel plant-derived adjuvant therapy for the treating photodamage.

Effect and mechanism of Tricholoma matsutake extract combined with bakuchiol and ergothioneine on UVB-induced skin aging.

Aging is a physiological phenomenon in the process of life, and skin aging has a significant impact on human appearance. Therefore, the search for methods to delay skin aging is of great significance for improving the quality of human life. This study investigated the anti-photoaging effect of Tricholoma matsutake (T) extract composition combined with bakuchiol (B) and ergothioneine (E), and explored its potential mechanism through transcriptome, metabolomics, and network pharmacology. 57 main chemical components are identified from the ethanol extract of T. matsutake (T), including D-carnitine (24.55%), α,α-trehalose (15.56%), DL malic acid (8.99%), D-(-)-quinic acid (7.46%), erucamide (7.04%) and so on. After TBE treatment, inflammation of the mice dorsal skin is significantly minimized. Hematoxylin and eosin (H&E) staining and toluidine blue staining reveal that TBE has an anti-inflammatory effect on the back skin tissue of mice. Masson staining shows that TBE has a repair effect on mice dorsal skin tissue. In addition, the inflammatory factors (IL-1β, IL-6, TNF-α) in the mice dorsal skin tissues are significantly reduced but collagen (COL-1) is significantly increased. By cellular immunofluorescence assay, TBE is shown to promote PPAR-α expression in cells. Transcriptomics, metabolomics, and network pharmacology have revealed that TBE can regulate exogenous stimuli and cancer-related signaling pathways to prevent skin aging. The results suggest that TBE can be a beneficial supplement to natural anti-aging.

Antioxidant peptide ETT from Isochrysis zhanjiangensis attenuate skin aging by maintaining homeostasis and promoting collagen generation

ETT (Glu-Met-Phe-Gly-Thr-Ser-Ser-Glu-Thr) isolated from Isochrysis zhanjiangensis was an antioxidant nonapeptide with the highest active site on Met 2. In this study, the investigated the anti-skin aging effect of ETT on both keratinocytes and fibroblasts, took ultraviolet B (UVB)-induced human immortalized keratinocytes (HaCaT) and hydrogen peroxide (H2O2)-induced human skin fibroblasts (BJ cells). The results showed the anti-photoaging effect of ETT on UVB-induced HaCaT cells by declining an increasing level of intracellular reactive oxygen species (ROS), activating antioxidant system via nuclear factor erythroid 2 (Nrf2)/ heme oxgenase-1 (HO-1) signaling pathway, promoting autophagy to enhancing mitochondrial membrane potential and inhibiting apoptosis. Moreover, ETT also against skin aging on H2O2-induced BJ cells by attenuating senescence and improving collagen generation via transforming growth factor β1 (TGF-β1)/Smad signaling pathway. In general, these results indicated ETT is potential to against skin aging by maintaining keratinocytes homeostasis, reducing apoptosis, attenuating fibroblasts senescence and enhancing content of collagen.

Synergistic delivery of hADSC-Exos and antioxidants has inhibitory effects on UVB-induced skin photoaging

Ultraviolet B (UVB) light exposure accelerates skin photoaging. Human adipose-derived stem cell exosomes (hADSC-Exos) and some antioxidants may have anti-photoaging effects. However, it is unknown whether the combination of hADSC-Exos and antioxidants plays a synergistic role in anti-photoaging. In cellular and 3D skin models, we showed that vitamin E (VE) and hADSC-Exos were optimal anti-photoaging combinations. In vivo, VE and hADSC-Exos increased skin tightening and elasticity in UVB-induced photoaging mice Combined treatment with VE and hADSC-Exos inhibited SIRT1/NF-κB pathway. These findings contribute to the understanding of hADSC-Exos in conjunction with other antioxidants, thereby providing valuable insights for the future pharmaceutical and cosmetic industries.

5-aminolevulinic acid photodynamic therapy protects against UVB-induced skin photoaging: A DNA-repairing mechanism involving the BER signalling pathway.

Low-dose 5-aminolevulinic acid photodynamic therapy (ALA-PDT) has been used to cope with skin photoaging, and is thought to involve DNA damage repair responses. However, it is still unknown how low-dose ALA-PDT regulates DNA damage repair to curb skin photoaging. We established a photoaging model using human dermal fibroblasts (HDFs) and rat skin. RNA-sequencing (RNA-seq) analysis was conducted to identify differentially expressed genes (DEGs) in HDFs before and after low-dose ALA-PDT treatment, followed by bioinformatics analysis. Senescence-associated β-galactosidase (SA-β-gal) staining was employed to assess skin aging-related manifestations and Western blotting to evaluate the expression of associated proteins. A comet assay was used to detect cellular DNA damage, while immunofluorescence to examine the expression of 8-hydroxy-2'-deoxyguanosine (8-oxo-dG) in cells and skin tissues. In both invivo and invitro models, low-dose ALA-PDT alleviated the manifestations of ultraviolet B (UVB)-induced skin photoaging. Low-dose ALA-PDT significantly reduced DNA damage in photoaged HDFs. Furthermore, low-dose ALA-PDT accelerated the clearance of the photoproduct 8-oxo-dG in photoaged HDFs and superficial dermis of photoaged rat skin. RNA-seq analysis suggested that low-dose ALA-PDT upregulated the expression of key genes in the base excision repair (BER) pathway. Further functional validation showed that inhibition on BER expression by using UPF1069 significantly suppressed SA-β-gal activity, G2/M phase ratio, expression of aging-associated proteins P16, P21, P53, and MUTYH proteins, as well as clearance of the photoproduct 8-oxo-dG in photoaged HDFs. Low-dose ALA-PDT exerts anti-photoaging effects by activating the BER signalling pathway.

Antioxidant, Anti-photoaging, and Anti-wrinkle Effects of Cosmetics Containing Low-molecular-weight Peptide Complexes

Purpose: This study aimed to confirm the skin improvement effects of cosmetics containing low-molecular-weight peptide complexes using <i>in vitro</i> and human application tests.Methods: An <i>in vitro</i> test was conducted to confirm the cytotoxicity, antioxidant, and anti-photoaging effects of cosmetics comprising low-molecular-weight peptide complexes. The protective effect on HacaT cells subjected to oxidative stress and collagen production in CCD-986sk cells irradiated with UV-B (Ultraviolet B) were confirmed. Moreover, to validate skin improvement effects, a human application test was performed on 20 adults aged 30–59 years. The wrinkles depth and the indentation index around the forehead, eyes, cheeks, and mouth were evaluated using ANTERA 3D CS.Results: The test material demonstrated excellent cell viability, confirming its safety on the skin. At a concentration of 0.1%, it exhibited a removal rate of reactive oxygen species (ROS) by 63.39% (<i>p</i><0.001) and an increase in collagen content of 102.14% (<i>p</i><0.01). Furthermore, in the human application test over 4 weeks, skin folds exhibited a decrease in average depth by 20.53% (<i>p</i><0.001), and the indentation index decreased by 17.02% (<i>p</i><0.001).Conclusion: Cosmetics containing low-molecular-weight peptide complexes possess excellent antioxidant, anti-photoaging, and collagen synthesis promotion properties. Their efficacy in reducing skin wrinkles and increasing skin elasticity was also confirmed. Low-molecular-weight peptide complexes could be an excellent active ingredient in cosmeceuticals.

The role and mechanism of engineered nanovesicles derived from hair follicle mesenchymal stem cells in the treatment of UVB-induced skin photoaging.

Extracellular vesicles (EVs) derived from mesenchymal stem cells (MSCs) are effective in the treatment of skin photoaging; however, their low yield and functional decline with passage progression limit their clinical application. Cell-derived nanovesicles (CNVs) are potential alternatives that can address the limitations of EVs derived from MSCs and are conducive to clinical transformations. Hair follicle mesenchymal stem cells (HFMSCs), a type of MSCs, have demonstrated the function of repairing skin tissues; nevertheless, the efficacy of CNVs from HFMSCs (HFMSC-CNVs) in the treatment of skin photoaging remains unclear. Therefore, ultraviolet radiation B (UVB)-induced photoaging nude mice and human dermal fibroblasts (HDFs) were used as experimental models to investigate the therapeutic effects of HFMSC-CNVs in photoaging models. HFMSC-CNVs were successfully prepared using the mechanical extrusion method. UVB-induced nude mice and HDFs were used as experimental models of photoaging. Multiple approaches, including hematoxylin-eosin and Masson staining, immunohistochemistry, immunofluorescence, detection of reactive oxygen species (ROS), flow cytometry, western blotting, and other experimental methods, were combined to investigate the possible effects and mechanisms of HFMSC-CNVs in the treatment of skin photoaging. In the nude mouse model of skin photoaging, treatment with HFMSC-CNVs reduced UVB-induced skin wrinkles (p < 0.05) and subcutaneous capillary dilation, alleviated epidermis thickening (p < 0.001), and dermal thinning (p < 0.001). Furthermore, HFMSC-CNVs upregulated proliferating cell nuclear antigen (PCNA) expression (p < 0.05) and decreased the levels of ROS, β-galactosidase (β-Gal), and CD86 (p < 0.01). Invitro experiments, treatment with HFMSC-CNVs enhanced the cellular activity of UVB-exposed HDFs (p < 0.05), and reduced ROS levels and the percentage of senescent cells (p < 0.001), and alleviated cell cycle arrest (p < 0.001). HFMSC-CNVs upregulated the expression of Collagen I (Col I), SMAD2/3, transforming growth factor beta (TGF-β), catalase (CAT), glutathione peroxidase-1 (GPX-1), and superoxide dismutase-1 (SOD-1) (p < 0.05) and downregulated the expression of cycle suppressor protein (p53), cell cycle suppressor protein (p21), and matrix metalloproteinase 3 (MMP3) (p < 0.05). Conclusively, the anti-photoaging properties of HFMSC-CNVs were confirmed both invivo and invitro. HFMSC-CNVs exert anti-photoaging effects by alleviating cell cycle arrest, decreasing cellular senescence and macrophage infiltration, promoting cell proliferation and extracellular matrix (ECM) production, and reducing oxidative stress by increasing the activity of antioxidant enzymes.

The extract of buds of Chrysanthemum morifolium ramat alleviated UVB-induced skin photoaging by regulating MAPK and Nrf2/ARE pathways

Ethnopharmacological relevanceChrysanthemum morifolium Ramat. is a commonly used Chinese herb and food homologous plant with traditional effects such as anti-inflammatory, antifebrile, antibacterial and antiviral. Aim of studyPhotoaging is one of the main causes of accelerated skin aging. Chrysanthemum morifolium Ramat. has reported to alleviate photodamage. In this study, we investigated the protective effect of the extract of buds of Chrysanthemum morifolium Ramat. (CE) on UVB-induced photoaging and further mechanism. Materials and methodsThe extract of buds of chrysanthemum was analyzed by HPLC-Q-TOF-MS/MS. Antioxidant activity was assessed by DPPH and ABTS assay. Cell viability examined by cell counting kit-8 assay. The ROS level was detected by fluorescent probe DCFH-DA. Protein expression evaluated by Western blotting. The skin tissue investigated by immunohistochemistry. ResultsCE significantly reversed the decrease of cell viability that induced by UVB in HaCaT and HFF-1 cells. Further analysis showed that CE alleviated photoaging by inhibiting the expression of mitogen-activated protein kinase (MAPK) and activating the NF-E2-related factor 2 (Nrf2)/antioxidant response element (ARE) pathway to promote the expression of antioxidant enzymes. Moreover, CE effectively improved the reduced skin hydration, disordered collagen and thickening epidermis caused by UVB in mice. ConclusionsAll results demonstrated that CE had therapeutic effect on UVB-induced photoaging and provided theoretical basis for its further developing as a natural functional product with anti-photoaging effect.

Anti-photoaging effects of steam-exploded pine (Pinus densiflora) extract in ultraviolet B irradiation-damaged HaCaT keratinocytes

Ultraviolet B (UVB) irradiation causes photoaging, such as wrinkles, roughness and dryness of the skin, and it activates the production of reactive oxygen species (ROS) and inflammatory cytokines. In this study, the anti-photoaging activity of SEP-E (steam-exploded pine extract) was evaluated in HaCaT keratinocytes damaged by UVB irradiation. SEP-E treatment showed cytoprotective effects in HaCaT keratinocytes irradiated with UVB (40 mJ/cm2). SEP-E treatment reduced ROS overproduction and promoted the expression of antioxidant enzymes, such as catalase, superoxide dismutase 1, and superoxide dismutase 2. Additionally, SEP-E treatment suppressed the expression of inflammatory cytokines, including interleukin 6, interleukin 8, and monocyte chemoattractant protein-1. Consequently, SEP-E shows potential as a natural material for photoaging treatment.

Salvianolic acid B protects against UVB-induced skin aging via activation of NRF2

BackgroundProlonged exposure to sun radiation may result in harmful skin photoaging. Therefore, discovering novel anti-photoaging treatment modalities is critical. An active component isolated from Salvia miltiorrhiza (SM), Salvianolic acid B (Sal-B), is a robust antioxidant and anti-inflammatory agent. This investigation aimed to discover the therapeutic impact and pathways of salvianolic acid B for UVB-induced skin photoaging, an area that remains unexplored. MethodsWe conducted in vitro experiments on human dermal fibroblasts (HDFs) exposed to UVB radiation, assessing cellular senescence, superoxide dismutase (SOD) activity, cell viability, proliferation, migration, levels of reactive oxygen species (ROS), and mitochondrial health. The potential mechanism of Sal-B was analyzed using RNA sequencing, with further validation through Western blotting, PCR, and nuclear factor erythroid 2-related factor 2 (NRF2) silencing methods. In vivo, a model of skin photoaging induced by UVB in nude mice was employed. The collagen fiber levels were assessed utilizing hematoxylin and eosin (H&E), Masson, and Sirus red staining. Additionally, NRF2 and related gene and protein expression levels were identified utilizing PCR and Western blotting. ResultsSal-B was found to significantly counteract photoaging in UVB-exposed skin fibroblasts, reducing aging-related decline in fibroblast proliferation and an increase in apoptosis. It was observed that Sal-B aids in protecting mitochondria from excessive ROS production by promoting NRF2 nuclear translocation. NRF2 knockdown experiments established its necessity for Sal-B's anti-photoaging effects. The in vivo studies also verified Sal-B's anti-photoaging efficacy, surpassing that of tretinoin (Retino-A). These outcomes offer novel insights into the contribution of Sal-B in developing clinical treatment modalities for UVB-induced photodamage in skin fibroblasts. ConclusionIn this investigation, we identified the Sal-B protective impact on the senescence of dermal fibroblasts and skin photoaging induced by radiation of UVB. The outcomes suggest Sal-B as a potential modulator of the NRF2 signaling pathway.

Centella asiatica transfersomes and Bergamot essential oil nanoemulsion combined in gel exhibited anti-photoaging effects on UVB-radiated BALB/c mice

Photoaging of skin tissue can result from exposure to ultraviolet B (UVB) radiation. This study developed two nanocarriers Centella asiatica (CA) transfersomes (TF) and Bergamot essential oil (BEO) nanoemulsions (NE) combined in a gel formulation as a drug delivery system, in order to study whether they could synergize to prevent UVB radiation and provide anti-photoaging effects. Nanoencapsulation of CA-TF and BEO-NE were examined for their quality by characterizing their physicochemical properties. An in vivo study evaluated topically applied CA-TF and BEO-NE combination gels biological effect on BALB/c mice before UVB radiation (840 mJ/cm2) for two weeks. Particle size analysis of developed nanocarriers exhibited monodispersed pattern with an average particle size and zeta potential of around 9.64 ± 0.35 nm and −39.86 ± 1.33 mV, respectively. In vivo experiments showed that topically applied CA-TF and BEO-NE combination gel significantly prevented UVB-induced wrinkle formation and skin erythema and inhibited histological damage, including epidermal hyperplasia, collagen fibers, and the destruction of elastic fibers. Additionally, the CA-TF and BEO-NE combination gel reduced UVB-induced oxidative stress by increasing superoxide dismutase (SOD) activity and suppressed lipid peroxidation by decreasing malondialdehyde (MDA) expression as well as inhibiting the expression of UVB-induced pro-inflammatory cytokines include tumor necrosis factor α (TNF-α) and interleukin 6 (IL-6). Moreover, the CA-TF and BEO-NE combination gel increased the type I collagen expression, restoring UVB-induced collagen production and density. Therefore, nanoencapsulation CA-TF and BEO-NE combination gel could synergistically prevent UVB-induced oxidative stress and inflammatory responses.

Skin-derived precursor conditioned medium alleviated photoaging via early activation of TGF-β/Smad signaling pathway by thrombospondin1: In vitro and in vivo studies

Photoaging is one major exogenous factor of skin aging. Efficacy and safety of current anti-photoaging therapies remained to be improved. Our previous studies indicated that skin-derived precursors (SKPs) alleviated photodamage by early activation of TGF-β/Smad signaling pathway via thrombospondin1 (TSP1). However, the research concerning SKP conditioned medium (SKP-CM) has never been reported. In the current study, we aimed to explore the anti-photoaging effects of SKP-CM both in vitro and in vivo, and to elucidate the possible mechanisms. Mouse SKP-CM (mSKP-CM) collection was optimized by a comparative method. The concentration of protein and growth factors in mSKP-CM was detected using BCA protein assay kit and growth factor protein chip. The anti-photoaging effects of mSKP-CM and its regulation of key factors in the TGF-β/Smad signaling pathway were explored using UVA + UVB photoaged mouse fibroblasts (mFBs) and nude mice dorsal skin. The research revealed that mSKP-CM contained significantly higher-concentration of protein and growth factors than mouse mesenchymal stem cell conditioned medium (mDMSC-CM). mSKP-CM alleviated mFBs photoaging by restoring cell viability and relieving senescence and death. ELISA, qRT-PCR, and western blot results implied the potential mechanisms were associated with the early activation of TGF-β/Smad signaling pathway by TSP1. In vivo experiments demonstrated that compared with the topical intradermal mDMSC-CM injection and retinoic acid cream application, the photodamaged mice dorsal skin intradermally injected with mSKP-CM showed significantly better improvement. Consistent with the in vitro results, both western blot and immunohistochemistry results confirmed that protein expression of TSP1, smad2/3, p-smad2/3, TGF-β1, and collagen I increased, and matrix metalloproteinases decreased. In summary, both in vitro and in vivo experiments demonstrated that mSKP-CM alleviated photoaging through an early activation of TGF-β/Smad signaling pathway via TSP1. SKP-CM may serve as a novel and promising cell-free therapeutical approach for anti-photoaging treatment and regenerative medicine.