UVB-induced Damage Research Articles

Maslinic acid attenuates UVB-induced oxidative damage in HFF-1 cells.

Oxidative damage is one of the major mechanisms of ultraviolet B (UVB)-induced damage to the skin. Maslinic acid (MA) is a natural compound of pentacyclic triterpene acids. It has been proved to have anti-inflammatory and antioxidant properties. This study aimed to explore the effects of MA on oxidative damage in human foreskin fibroblast cells (HFF-1) and the potential molecular mechanisms. A specific dose of UVB radiation was used to induce oxidative damage in HFF-1. Based on this, we performed measurements of cell proliferation, reactive oxygen species (ROS) levels, antioxidant enzyme activity, inflammation-related mediators, and NF-κB nuclear localization with or without the addition of MA. MA significantly promoted cell proliferation viability at 10 and 20 μM. The addition of MA 24 h before UVB irradiation was more effective at enhancing cell proliferation and also produced lower ROS levels compared to co-cultured fibroblasts and MA for 24 h after irradiation. However, there was no statistically significant difference between groups at concentrations of 10 and 20 μM. The pretreatment group with MA had elevated superoxide dismutase and catalase activities, decreased IL-6 generation, and lowered mRNA levels of IL-6, TNF-α and MMP3 in comparison with the UVB-irradiated group without additional MA. Meanwhile, the nuclear translocation of NF-κB and the degradation of IκB were inhibited by MA pretreatment. Taken together, these findings suggest that MA may alleviate UVB-induced oxidative damage in HFF-1 by inhibiting the nuclear translocation of NF-κB.

Protective Effect of Castanopsis sieboldii Extract against UVB-Induced Photodamage in Keratinocytes.

Ultraviolet B (UVB) rays disrupt the skin by causing photodamage via processes such as reactive oxygen species (ROS) production, endoplasmic reticulum (ER) stress, DNA damage, and/or collagen degradation. Castanopsis sieboldii is an evergreen tree native to the southern Korean peninsula. Although it is known to have antioxidant and anti-inflammatory effects, its protective effect against photodamage in keratinocytes has not been investigated. Thus, in the present study, we investigated the effect of 70% ethanol extract of C. sieboldii leaf (CSL3) on UVB-mediated skin injuries and elucidated the underlying molecular mechanisms. CSL3 treatment restored the cell viability decreased by UVB irradiation. Moreover, CSL3 significantly inhibited UVB- or tert-butyl hydroperoxide-mediated ROS generation in HaCaT cells. ER stress was inhibited, whereas autophagy was upregulated by CSL3 treatment against UVB irradiation. Additionally, CSL3 increased collagen accumulation and cell migration, which were decreased by UVB exposure. Notably, epigallocatechin gallate, the major component of CSL3, improved the cell viability decreased by UVB irradiation through regulation of ER stress and autophagy. Conclusively, CSL3 may represent a promising therapeutic candidate for the treatment of UVB-induced skin damage.

Myricetin Nanofibers Enhanced Water Solubility and Skin Penetration for Increasing Antioxidant and Photoprotective Activities.

Excessive exposure to ultraviolet radiation (UV) can induce oxidative stress through the over-production of reactive oxygen species (ROS) on the skin. Myricetin (MYR), a natural flavonoid compound, significantly inhibited UV-induced keratinocyte damage; however, its bioavailability is limited by its poor water solubility and inefficient skin penetration ability, which subsequently influences its biological activity. The purpose of the study was to develop a myricetin nanofibers (MyNF) system of hydroxypropyl-β-cyclodextrin (HPBCD)/polyvinylpyrrolidone K120 (PVP)-loaded with MYR that would enhance the water solubility and skin penetration by changing the physicochemical characteristics of MYR, including reducing the particle size, increasing the specific surface area, and amorphous transformation. The results also revealed that the MyNF can reduce cytotoxicity in HaCaT keratinocytes when compared with MYR; additionally, MyNF had better antioxidant and photoprotective activity than raw MYR for the UVB-induced HaCaT keratinocytes damage model due to the MyNF increased water solubility and permeability. In conclusion, our results demonstrate that MyNF is a safe, photostable, and thermostable topical ingredient of antioxidant nanofibers to enhance the skin penetration of MYR and prevent UVB-induced skin damage.

Effects of donkey milk on UVB-induced skin barrier damage and melanin pigmentation: A network pharmacology and experimental validation study.

Dairy products have long been regarded as a controversial nutrient for the skin. However, a clear demonstration of donkey milk (DM) on skincare is required. In this study, spectrum and chemical component analyses were applied to DM. Then, the effects of DM on UVB-induced skin barrier damage and melanin pigmentation were first evaluated in vitro and in vivo. Cell survival, animal models, and expression of filaggrin (FLG) were determined to confirm the effect of DM on UVB-induced skin barrier damage. Melanogenesis and tyrosinase (TYR) activity were assessed after UVB irradiation to clarify the effect of DM on whitening activities. Further, a network pharmacology method was applied to study the interaction between DM ingredients and UVB-induced skin injury. Meanwhile, an analysis of the melanogenesis molecular target network was developed and validated to predict the melanogenesis regulators in DM. DM was rich in cholesterols, fatty acids, vitamins and amino acids. The results of evaluation of whitening activities in vitro and in vivo indicated that DM had a potent inhibitory effect on melanin synthesis. The results of effects of DM on UVB‑induced skin barrier damage indicated that DM inhibited UVB-induced injury and restored skin barrier function via up-regulation expression of FLG (filaggrin). The pharmacological network of DM showed that DM regulated steroid biosynthesis and fatty acid metabolism in keratinocytes and 64 melanin targets which the main contributing role of DM might target melanogenesis, cell adhesion molecules (CAMs), and Tumor necrosis factor (TNF) pathway. These results highlight the potential use of DM as a promising agent for whitening and anti-photoaging applications.

Prevention and Repair of Ultraviolet B-Induced Skin Damage in Hairless Mice via Transdermal Delivery of Growth Factors Immobilized in a Gel-in-Oil Nanoemulsion.

Ultraviolet (UV) radiation from the sun or artificial sources is one of the primary causes of skin damage, including sunburns, tanning, erythema, and skin cancer. Among the three different types of UV rays, UVB rays have a medium wavelength that can penetrate the epidermal layer of the skin, resulting in sunburn, suntan, blistering, and melanoma in case of chronic exposure. This study aimed to evaluate the preventive and therapeutic effects of a gel-in-oil nanogel dispersion (G/O-NGD) as a transdermal delivery biomolecular carrier for skin damage caused by UVB light. The efficacy of this carrier against UVB-induced skin damage was investigated in vivo by delivering different growth factors (GFs) encapsulated in a G/O-NGD. Artificial UVB light was used to induce skin damage in nude mice, followed by the transdermal application of five GF [vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), epidermal growth factor (EGF), transforming growth factor (TGF)-1, and insulin-like growth factor (IGF)-α]-immobilized G/O-NGD. Among these GFs, VEGF and bFGF promoted angiogenesis, while EGF, TGF-1, and IGF-α promoted the repair and regeneration of damaged cells. The results showed that G/O-NGD was superior to heparin-immobilized G/O-NGD in reducing UVB-induced skin damage, such as erythema, epidermal water reduction, inflammation, and dermis thickening. In addition, G/O-NGD could prevent and treat abnormal follicle proliferation caused by UVB rays and exhibited potential to repair lipid glands. Overall, our results demonstrate the potential of G/O-NGDs for the treatment of UVB-induced skin damage.

Co-Regulatory Roles of WC1 and WC2 in Asexual Development and Photoreactivation of Beauveria bassiana.

The white collar proteins WC1 and WC2 interact with each other to form a white collar complex acting as a well-known transcription regulator required for the operation of the circadian clock in Neurospora, but their roles in insect-pathogenic fungal lifecycles remain poorly understood. Here, we report that WC1 and WC2 orthologs co-regulate the conidiation capacity and conidial resistance to solar ultraviolet-B (UVB) irradiation in Beauveria bassiana, after their high activities in the photorepair of UVB-induced DNA damages were elucidated previously in the insect mycopathogen, which features non-rhythmic conidiation and high conidiation capacity. The conidial yield, UVB resistance, and photoreactivation rate of UVB-impaired conidia were greatly reduced in the null mutants of wc1 and wc2 compared to their control strains. However, many other lifecycle-related phenotypes, except the antioxidant response, were rarely affected in the two mutants. Transcriptomic analysis revealed largely overlapping roles for WC1 and WC2 in regulating the fungal gene networks. Most of the differentially expressed genes identified from the null mutants of wc1 (1380) and wc2 (1001) were co-downregulated (536) or co-upregulated (256) at similar levels, including several co-downregulated genes required for aerial conidiation and DNA photorepair. These findings expand a molecular basis underlying the fungal adaptation to solar UV irradiation and offer a novel insight into the genome-wide co-regulatory roles of WC1 and WC2 in B. bassiana's asexual development and in vivo photoreactivation against solar UV damage.

Succinoglycan riclin relieves UVB-induced skin injury with anti-oxidant and anti-inflammatory properties

Excessive UVB exposure increases the production of reactive oxygen species (ROS), which causes oxidative damage and epidermal inflammation. Previous studies have identified that the succinoglycan riclin has potent anti-inflammatory properties. The current study aims to investigate whether riclin protects against UVB-induced photodamage. In vitro, riclin demonstrated excellent moisture-preserving properties, along with antioxidant potential by scavenging superoxide anions, hydroxyl and DPPH radicals. Riclin increased Col1α1 and Col3α1 expression in NIH3T3 cells, inhibited oxidation and melanin synthesis by B16F10 cells upon UVB irradiation. In vivo, topical application of riclin effectively attenuated UVB-induced skin damage in C57BL6 mice, which was characterized by erythema, epidermal hyperplasia, hydroxyproline loss and ROS production in skin tissue. Riclin suppressed skin inflammation by the elevation of TNF-α, IL-6, IL-β, and alleviated UVB-induced immune cell up-regulation. Moreover, treatment with a Dectin-1 inhibitor reversed the protective effect of riclin in THP-1 cells.

Identification of potential immune-related ceRNA Regulatory Network in UVB-irradiated human skin

ABSTRACT For a better understanding the molecular biomarkers in UVB-induced skin damage, and its potential mechanism, we downloaded two microarray data sets on skin UVB damage from the Gene Expression Omnibus (GEO): GSE21429, GSE56754. By using the Limma package to analyze differential gene expression and co-expression network analysis to screen module genes, 16 common genes were identified (16 up-regulated). Gene Ontology analysis to explore the functional roles of these genes indicated that the common genes were associated mainly with melanin biosynthetic process and metabolic process. Gene Set Enrichment Analysis provided evidence that the most gene sets enriched in immune and inflammation-related signaling pathways in the UVB-treated subjects, as compared with the untreated subjects. The PPI network genes were ranked according to the degree of connectivity, the top three ranked genes: ”MLANA”, ”GPR143” and ”SFTPC” were identified as potential biomarkers using the area under the receiver operating characteristic curve. The relative proportion of 22 immune cell types was then calculated by using the CIBERSORT algorithm. A higher follicular helper T cell ratio in UVB-treated samples compared to untreated samples was observed. Moreover, three hub genes have also been shown to be associated with immune cells. Finally, through multiple online miRNA databases, we propose MLANA-miR-573-MALAT1/NEAT1, GPR143-miR-138-5p-MALAT1/ KCNQ1OT1 might be potential RNA regulatory pathways that control disease progression in UVB-induced skin damage. In summary, the present results provide novel insights into the UVB-radiation related biological process changes, and further offer a new clinical application for prognosis and diagnostic prediction of UVB radiation-mediated skin damage.

Improvement of Therapeutic Value of Quercetin with Chitosan Nanoparticle Delivery Systems and Potential Applications

This paper reviews recent studies investigating chitosan nanoparticles as drug delivery systems for quercetin. The therapeutic properties of quercetin include antioxidant, antibacterial and anti-cancer potential, but its therapeutic value is limited by its hydrophobic nature, low bioavailability and fast metabolism. Quercetin may also act synergistically with other stronger drugs for specific disease states. The encapsulation of quercetin in nanoparticles may increase its therapeutic value. Chitosan nanoparticles are a popular candidate in preliminary research, but the complex nature of chitosan makes standardisation difficult. Recent studies have used in-vitro, and in-vivo experiments to study the delivery of quercetin alone or in combination with another active pharmaceutical ingredient encapsulated in chitosan nanoparticles. These studies were compared with the administration of non-encapsulated quercetin formulation. Results suggest that encapsulated nanoparticle formulations are better. In-vivo or animal models simulated the type of disease required to be treated. The types of diseases were breast, lung, liver and colon cancers, mechanical and UVB-induced skin damage, cataracts and general oxidative stress. The reviewed studies included various routes of administration: oral, intravenous and transdermal routes. Although toxicity tests were often included, it is believed that the toxicity of loaded nanoparticles needs to be further researched, especially when not orally administered.

Enhancement of Human Epidermal Cell Defense against UVB Damage by Fermentation of Passiflora edulis Sims Peel with Saccharomyces cerevisiae.

The processing of Passiflora edulis Sims results in large amounts of wasted peel resources and environmental pollution. In order to improve the utilisation of natural plant resources and economic benefits, this study uses Saccharomyces cerevisiae to ferment Passiflora edulis Sims peel to obtain Passiflora edulis Sims peel fermentation broth (PF). The content of active substances in unfermented Passiflora edulis Sims peel water extract (PW) and PF is then determined, as well as their in vitro antioxidant capacity. The protective effects of PF and PW on UVB-induced skin inflammation and skin barrier damage in human immortalised epidermal keratinocytes (HaCaT) cells (including cell viability, ROS, HO-1, NQO1, IL-1β, IL-8, TNF-α, KLK-7, FLG, AQP3 and Caspase 14 levels) are investigated. Studies have shown that PF enhances the content of active substances more effectively compared to PW, showing a superior ability to scavenge free radical scavenging and antioxidants. PW and PF can effectively scavenge excess intracellular ROS, reduce the cellular secretion of pro-inflammatory factors, regulate the content of skin barrier-related proteins and possibly respond to UVB-induced cell damage by inhibiting the activation of the PI3K/AKT/mTOR signalling pathway. Studies have shown that both PW and PF are safe and non-irritating, with PF exploiting the efficacy of Passiflora edulis Sims peel more significantly, providing a superior process for the utilisation of Passiflora edulis Sims waste. At the same time, PF can be developed and used as a functional protective agent against ultraviolet damage to the skin, thereby increasing the value of the use of Passiflora edulis Sims waste.

Hemin protects UVB-induced skin damage through inhibiting keratinocytes apoptosis and reducing neutrophil infiltration.

Ultraviolet-B (UVB) exposure on the skin triggers apoptosis, oxidative stress and acute inflammatory responses, which eventually increases the risk of various skin disorders. Hemin, an iron-binding porphyrin, has been clinically used for porphyria treatment. However, whether hemin contributes to the skin protection against UVB injury remains to be elucidated. Here, we found that hemin treatment (10 and 20mg/kg) by intraperitoneal administration could dramatically relieve UVB irradiation-induced skin damage featured by erythema, edema, epidermal hyperplasia and collagen loss in C57BL/6J mice. Importantly, hemin treatment attenuated UVB irradiation-triggered cell apoptosis in skin epidermis. Consistently, hemin (10, 20μM) treatment decreased Caspase-3 activation and protected against UVB-induced apoptosis in HaCaT cells. Besides, hemin treatment reduced the infiltration of neutrophils in skin under UVB irradiation, thus restrained neutrophil extracellular traps (NET) formation and myeloperoxidase (MPO) release. We further revealed that hemin inhibited the expression of inflammation associated cytokines and chemokines in UVB-induced HaCaT cells and blocked the chemotaxis of dHL-60 cells to preconditioned media from HaCaT culture upon UVB irradiation. Furthermore, hemin inhibited the excessive maturation and mobilization of bone marrow neutrophils and rectified the proportion of abnormally elevated neutrophils in the blood under UVB irradiation. In conclusion, our study showed that hemin treatment protects against UVB-induced skin damage through inhibiting keratinocytes apoptosis, and suppressing neutrophils infiltration in the skin via externally restraining the keratinocyte attraction and internally regulating bone marrow neutrophil maturation and mobilization, suggesting that hemin is an effective drug candidate for the therapy of UVB damage.

Protective effect of novel strain of Pleurotus sp. on UVB-induced skin damage: Involvement of antioxidant ergothioneine and its transporter SLC22A4

Protective effect of novel strain of Pleurotus sp. on UVB-induced skin damage: Involvement of antioxidant ergothioneine and its transporter SLC22A4

The Effect of Elasticity Improvement from Acetyl Hexapeptide-8 Ampoule on UVB-Induced Mouse Skin Damage

Acetyl hexapeptide-8 (AH-8) is a well-known component of anti-aging products. AH-8 appears in a variety of cosmetic products, its skin penetration is sparsely studied and controversially discussed. This study investigated ampoule containing AH-8 as an active ingredient. The elasticity improving effect of 3% AH-8 ampoule was tested <i>in vivo</i>. To test the stability of the formulated ampoules, we performed the centrifugation, cycling and measured viscosity, and pH changes. 6 weeks-old female C3H mice were purchased from Orient Bio, Korea Inc. (Seongnam, Korea). After one week of acclimatization, the mice were randomly assigned to experimental groups (n=4 for each group); Control, UVB irradiation, Vehicle ampoule, and 3% AH-8 ampoule group. Irradiated with UVB to mouse skin, then 3% AH-8 ampoule were applied into irradiated sites for 6 weeks. Changes in the amount of TGF-β1 and collagen were measured using western blot. As a result, it was confirmed that the 3% AH-8 ampoule increased the expression of TGF-β1 and collagen. In summary, we showed that AH-8 ampoule had extremely high capability of improving elasticity when compared to vehicle ampoule containing ginkgo leaf and green tea extracts. This study revealed the efficacy of AH-8 for increasing skin elasticity and anti-aging in terms of a cosmetic active ingredient.

Andrographolide protects acute ultraviolet-B radiation-induced photodamages in the mouse skin.

This study evaluates the preventive role of andrographolide (ADP) against ultraviolet-B (UVB) radiation-induced photoaging in the mouse skin. Grouped mice were subjected to UVB irradiation at the dose of 180mJ/cm2 for ten consecutive days. The ADP (3.6mgkg/b.wt) was topically administrated 1h before each UVB-irradiation. We observed that UVB irradiation enhances lipid peroxidative thiobarbituric acid reactive substances (TBARS) and attenuated antioxidant enzyme activities in the mouse skin. Conversely, the ADP pretreatment reversed the lipid peroxidation and restored antioxidant status in the mouse skin. Histological observations clearly show the preventive effect of ADP against UVB-induced dermal tissue damage. Further, ADP slow-down the UVB-mediated expression of inflammatory proteins such as CD34, iNOS, NF-κB COX-2, IL-6, and IL-10 in the mouse skin. Moreover, western blotting studies revealed that ADP prevents UVB exposure-mediated apoptosis markers p53 overexpression in the mouse skin. Thus, ADP protects mouse skin from UVB radiation exposure through impeding inflammation, oxidative stress, and apoptosis.

Preparation of CPD Photolyase Nanoliposomes Derived from Antarctic Microalgae and Their Effect on UVB-Induced Skin Damage in Mice.

UVB radiation is known to trigger the block of DNA replication and transcription by forming cyclobutane pyrimidine dimer (CPD), which results in severe skin damage. CPD photolyase, a kind of DNA repair enzyme, can efficiently repair CPDs that are absent in humans and mice. Although exogenous CPD photolyases have beneficial effects on skin diseases, the mechanisms of CPD photolyases on the skin remain unknown. Here, this study prepared CPD photolyase nanoliposomes (CPDNL) from Antarctic Chlamydomonas sp. ICE-L, which thrives in harsh, high-UVB conditions, and evaluated their protective mechanisms against UVB-induced damage in mice. CPDNL were optimized using response surface methodology, characterized by a mean particle size of 105.5 nm, with an encapsulation efficiency of 63.3%. Topical application of CPDNL prevented UVB-induced erythema, epidermal thickness, and wrinkles in mice. CPDNL mitigated UVB-induced DNA damage by significantly decreasing the CPD concentration. CPDNL exhibited antioxidant properties as they reduced the production of reactive oxygen species (ROS) and malondialdehyde. Through activation of the NF-κB pathway, CPDNL reduced the expression of pro-inflammatory cytokines including IL-6, TNF-α, and COX-2. Furthermore, CPDNL suppressed the MAPK signaling activation by downregulating the mRNA and protein expression of ERK, JNK, and p38 as well as AP-1. The MMP-1 and MMP-2 expressions were also remarkably decreased, which inhibited the collagen degradation. Therefore, we concluded that CPDNL exerted DNA repair, antioxidant, anti-inflammation, and anti-wrinkle properties as well as collagen protection via regulation of the NF-κB/MAPK/MMP signaling pathways in UVB-induced mice, demonstrating that Antarctic CPD photolyases have the potential for skincare products against UVB and photoaging.

Streptomyces spp. Isolated from Rosa davurica Rhizome for Potential Cosmetic Application

Streptomyces species are widely studied and used in different fields, including antibiotics and pesticides, and are spread in several places as soil-derived microorganisms. However, research on anti-aging, including antioxidants obtained from Streptomyces, has not been performed as much. Skin aging due to bacterial infection, especially methicillin-resistant Staphylococcus aureus (MRSA), is challenging to recover, so it is essential to prevent aging by preventing or inhibiting infection. Therefore, this study was conducted to isolate Streptomyces species from Rosa davurica rhizome soil and to determine the effect of the ethyl acetate extract of the isolated strain Streptomyces chattanoogensis THA-663 (THA-663S) on the inhibition of MRSA and UVB-irradiated human skin keratinocytes, to determine whether it could be a treatment for skin aging. The MRSA inhibition and antioxidant activities were evaluated using disc diffusion, 2,2-diphenyl-1-picrylhydrazyl (DPPH), 2,2’-azino-bis-(3-ethylbenzothiazoline)-6-sulfonic acid (ABTS), and a reactive oxygen species (ROS) assay. The expression of aging-related markers, including mitogen-activated protein kinases/activator protein 1 (MAPK)/AP-1) and transforming growth factor-β/suppressor of mothers against decapentaplegic (TGF-β/Smad) was assessed using Western blotting. The antibacterial effect on four MRSA strains, CCARM 0204, CCARM 0205, CCARM 3855, and CCARM 3089, showed that THA-663S could greatly inhibit MRSA growth. Moreover, the findings showed that THA-663S is efficient in scavenging free radicals and dose-dependently reducing ROS generation. Furthermore, THA-663S notably reduced UVB-induced matrix metalloproteinase-1 (MMP-1) expression by inhibiting the MAPK/AP-1 signaling pathways and blocking extracellular matrix (ECM) degradation in UVB-irradiated HaCaT cells. Additionally, THA-663S improved and enhanced transforming growth factor-beta (TGF-β) signaling activation to promote procollagen type I synthesis, relieving UVB-induced skin cell damage. In conclusion, THA-663S has a high potential to protect skin cells from aging, and, simultaneously, it can prevent or treat aging caused by infection due to pathogen inhibition.

IN-VITRO MELANOGENESIS, CYTOTOXICITY AND ANTIOXIDANT ACTIVITIES OF Peltophorum pterocarpum LEAF EXTRACTS

Melanin is a protective pigment against cellular damage and skin cancer. Peltophorum pterocarpum has been used for centuries to treat skin diseases like eczema and psoriasis. However, whether P. pterocarpum leaf extract can affect melanin synthesis with the advantage of antioxidant defense against ultraviolet (UV) radiation remains to be investigated. We aimed to examine the melanogenesis, cytotoxicity, and antioxidant activities of P. pterocarpum leaf extracts. A two-dimensional (2D) cell culture model was employed to demonstrate the effect of P. pterocarpum extracts on melanin synthesis. The cell viability of B16-F1 melanoma cells was measured by Neutral Red Uptake (NRU) assay. Antioxidant activity was accessed using 2,2-diphenyl-1-picrylhydrazyl (DPPH) and 2’,7’-dichlorodihydrofluorescein diacetate (DCFH-DA) assays. The ethanol extract of P. pterocarpum dose-dependently increased the melanin content and displayed cytotoxicity to B16-F1 melanoma cells at the highest concentration. In contrast, the equal amounts of the aqueous extract significantly inhibited melanin synthesis and did not show any cytotoxic effects on B16-F1 melanoma cells. The P. pterocarpum ethanol extract had a significantly higher total phenolic and flavonoid content than the aqueous extract and was more effective at scavenging DPPH free radicals and intracellular ROS induced by UVB, with IC50 of 519.24 ± 122.57 vs 1798.45 ± 143.09 µg/mL and 878.00 ± 23.50 vs 1379.00 ± 21.81 µg/mL, respectively. These findings suggest that the pro-melanogenic and anti-melanogenic activities of P. pterocarpum extract with antioxidant capacity against UVB-induced cellular damage are affected by the total phenolic and flavonoid contents.

PHOTOPROTECTIVE EFFECTS OF CARRAGEENANS AGAINST ULTRAVIOLETB-INDUCED EXTRACELLULAR MATRIX (ECM) DAMAGE IN KERATINOCYTES

Carrageenans, the polysaccharide from red seaweeds is widely used in food, medicine and as an excipient in cosmetics and skincare products. Carrageenans have shown prospective photoprotective effect against ultraviolet B (UVB) irradiation on immortalised normal human keratinocyte (HaCaT) cells. The aim of this research was to evaluate the photoprotective effect of iota (ι), kappa (κ)-carrageenans and their combination with vitamin E against UVB-induced extracellular matrix (ECM) damage in HaCaT cells. The study also assessed the superoxide dismutase (SOD) and catalase (CAT) antioxidant enzymes in UVB exposed pre-treated and non-pre-treated cells. The parameters assessed were biological mediators important for the structural integrity of ECM, comprising of epidermal growth factor receptor (EGFR), mitogen-activated protein kinase (MAPK), activating protein- (AP-1) and matrix metalloproteinases (MMPs), liberated by the UVB exposed cells. Enzyme linked immunosorbent assay was used to evaluate the release of these mediators. Carrageenans enhanced the activities of the antioxidant enzymes SOD and CAT which acts as a defence mechanism against oxidative stress. The levels of the biological mediators were also reduced in cells pre-treated with carrageenans, suggesting that the polysaccharide has potential in maintaining the skin’s integrity by reducing the damage to ECM upon UVB exposure. Taken together, the results suggest that carrageenans do possess photoprotective effects against UVB-induced ECM damage and stimulates antioxidant enzymes.

Two Laminaria japonica Fermentation Broths Alleviate Oxidative Stress and Inflammatory Response Caused by UVB Damage: Photoprotective and Reparative Effects.

UVB radiation can induce oxidative stress and inflammatory response in human epidermal cells. We establish a UVB-induced damage model of human immortalized epidermal keratinocytes (HaCaT) to explore the protective and reparative effects of Laminaria japonica on UVB-damaged epidermal inflammation after fermentation by white Ganoderma lucidum (Curtis) P. Karst and Saccharomyces cerevisiae. Compared with unfermented Laminaria japonica, fermented Laminaria japonica possesses stronger in vitro free radical scavenging ability. Laminaria japonica white Ganoderma lucidum fermentation broth (LJ-G) and Laminaria japonica rice wine yeast fermentation broth (LJ-Y) can more effectively remove excess reactive oxygen species (ROS) in cells and increase the content of the intracellular antioxidant enzymes heme oxygenase-1 (HO-1) and NAD(P)H quinone oxidoreductase 1 (NQO-1). In addition, fermented Laminaria japonica effectively reduces the content of pro-inflammatory factors ILs, TNF-α and MMP-9 secreted by cells. The molecular research results show that fermented Laminaria japonica activates the Nrf2 signaling pathway, increases the synthesis of antioxidant enzymes, inhibits the gene expression levels of pro-inflammatory factors, and alleviates cellular oxidative stress and inflammatory response caused by UVB radiation. Based on the above results, we conclude that fermented Laminaria japonica has stronger antioxidant and anti-inflammatory activity than unfermented Laminaria japonica, possesses good safety, and can be developed and used as a functional inflammation reliever. Fermented Laminaria japonica polysaccharide has a more slender morphological structure and more rockulose, with better moisturizing and rheological properties.

Conditioned Medium from H2O2-Preconditioned Human Adipose-Derived Stem Cells Ameliorates UVB-Induced Damage to Human Dermal Fibroblasts.

Human skin exposure to ultraviolet B (UVB) radiation can result in acute photodamage through oxidative modifications of cellular components and biomolecules involved in the metabolism of dermal cells. Recently, the therapeutic potential of human adipose-derived stem cells (hASCs) has been investigated as a novel strategy for photoprotection due to their pro-angiogenic properties, protective activity against oxidative stress and paracrine effect on dermal cells. To enhance these therapeutic properties, hASCs can be preconditioned by exposing them to sublethal cellular stressors. In this study, we first analyzed response capacity against UVB-induced oxidative stress in H2O2-preconditioned hASCs (called HC016 cells); and second, we evaluated the photoprotective effect of HC016-conditioned medium (CM) in an in vitro UVB irradiation model in cultured human foreskin fibroblasts (hFFs). The results demonstrated that HC016 cells have a greater capacity to respond efficiently to UVB-induced oxidative stress, evidenced by higher Nrf2 antioxidant system activity and enhanced viability and migration capacity. Further, HC016-CM treatment increased viability, migratory capacity and collagen type I synthesis in hFFs exposed to UVB radiation, as well as reducing their cytotoxicity, apoptosis, senescence and IL-6 secretion. Collectively, these findings support the view that HC016 cells could protect against UVB-induced photodamage via paracrine mechanisms.