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Sunscreen products can protect the skin against the harmful effects of UV radiation, including reddening, aging, and cancer. The aim of this research was to evaluate the photoprotective effects of yeast pulcherrimin, an iron-chelating dipeptide. We first investigated the cytotoxicity of pulcherrimin produced by Metschnikowia pulcherrima yeast on the human keratinocyte HaCaT cell line, using the PrestoBlue assay. We assessed the ability of pulcherrimin to induce DNA repair after the exposure of HaCaT cells to oxidative stress. We also evaluated its protective activity against UVC radiation. The sun protective factor (SPF) was calculated using the Mansur equation. The UVA/UVB ratio values for pure pulcherrimin were evaluated using the Boots Star Rating system. The critical wavelength was determined by calculating the integrated optical density curve area. Based on the results, pulcherrimin shows strong cytoprotective effects through antioxidant and photoprotective activities on the HaCaT cell line. The calculated SPFs were 20 and 15 at pH = 7 and pH = 10, respectively. The critical wavelength above 370 nm and the UVA/UVB ratio R > 1 suggest that yeast pulcherrimin—a cyclic dipeptide containing iron—may be considered a promising photoprotective agent. [ABSTRACT FROM AUTHOR]

To improve the utilization of by-products of the Hyriopsis cumingii, this study investigated the effect of Hyriopsis cumingii polysaccharide (HCP) on the proliferation and migration of normal cells, as well as its reparative effects on ultraviolet radiation-B (UVB)-damaged cells. First, HCP was isolated and purified using DEAE Cellulose-52 column chromatography, Sephadex G-100 column chromatography and nanofiltration. Then, structural analysis was conducted using high-performance liquid chromatography, high-performance gel permeation chromatography, and infrared spectroscopy. Following this, cell proliferation experiments, cell scratch tests, UVB damage experiments, and protein expression analyses were employed to explore the anti-UVB damage effects and corresponding mechanisms of polysaccharide components. The results indicated the three substances obtained by isolation and purification were all homogeneous polysaccharide components. Among them, HCP-2 played a major role in promoting cell proliferation in HCP and facilitated the migration of HaCaT cells. The recovery of UVB-damaged cell vitality was raised by the increasing concentration of HCP-2. Furthermore, the reparative effect was more substantial than the protective effect at the same sample concentration. It was also observed that HCP-2 up-regulated the expression of the anti-apoptotic protein bcl-2 while inhibited the expression of apoptosis-related proteins casp9, p-Akt, and p-p38, indicating that HCP-2 could repair HaCaT cells by regulating apoptosis of cells damaged by UVB. In conclusion, HCP had the ability to inhibit cell apoptosis which provide a theoretical basis for its future application in the development of food and health products. [ABSTRACT FROM AUTHOR]

Abalone, a marine edible gastropod with nutritional value, is a popular seafood delicacy worldwide, especially in Asia; however, viscera by-products are generally discarded during processing. Therefore, we investigated the skin health benefits of abalone viscera ultrasonic extract (AVU) in human dermal fibroblasts (HDFs) and human keratinocyte (HaCaT) cells. AVU showed valuable protein contents, indicating that it is a worthy and safe material for industrial application. AVU increased collagen synthesis production and messenger RNA (mRNA) expression of Collagen Type I Alpha 1, 2, and 3 chains through the transforming growth factor beta/suppressor of mother against the decapentaplegic pathway in HDF cells. AVU also increased hyaluronic acid production, upregulated Hyaluronan Synthases 1, 2, and 3, filaggrin and aquaporin3 mRNA levels, and downregulated hyaluronidase mRNA levels in HaCaT cells. Furthermore, mechanistic studies showed that AVU increased the phosphorylation of extracellular signal-regulated kinase, p38, and cyclic AMP response-binding protein activation. AVU activated the transcription factors, phosphoinositide 3-kinase, protein kinase B, and nuclear factor kappa B cell p65 and downregulated the degranulation of inhibitory kappa B in HaCaT cells. Studies of hyaluronic acid production in AVU by inhibiting EKR, p38 and NF-κB have shown that p38 MAPK and NF-κB signaling are pivotal mechanisms, particularly in the AVU. These results demonstrated that AVU produced from by-products may improve skin health and may thus be used as a functional food and cosmetics ingredient. [ABSTRACT FROM AUTHOR]

Porphyrazines (Pzs) are porphyrin derivatives that show potential application as photosensitizers for photodynamic therapy (PDT), but are still far less explored in the literature. In this work, we evaluate how the photophysics and phototoxicity of the octakis(trifluoromethylphenyl)porphyrazine (H2Pz) against tumor cells can be modulated by coordination with Mg(II), Zn(II), Cu(II) and Co(II) ions. Fluorescence and singlet oxygen quantum yields for the Pzs were measured in organic solvents and in soy phosphatidylcholine (PC) liposomes suspended in water. While H2Pz and the respective complexes with Cu(II) and Co(II) showed very low efficiency to fluoresce and to produce 1O2, the Mg(II) and Zn(II) complexes showed significantly higher quantum yields in organic solvents. The fluorescence of these two Pzs in the liposomes was sensitive to the fluidity of the membrane, showing potential use as viscosity markers. The cytotoxicity of the compounds was tested in HaCaT (normal) and A431 (tumor) cells using soy PC liposomes as drug carriers. Despite the low 1O2 quantum yields in water, the Mg(II) and Zn(II) complexes showed IC50 values against A431 cells in the nanomolar range when activated with low doses of red LED light. Their phototoxicity was ca. three times higher for the tumor cells compared to the normal ones, showing promising application as photosensitizers for PDT protocols. Considering that H2Pz and the respective Co(II) and Cu(II) complexes were practically non-phototoxic to the cells, we demonstrate the importance of the central metal ion in the modulation of the photodynamic activity of porphyrazines. [ABSTRACT FROM AUTHOR]

Extended exposure to UVB (280–315 nm) radiation results in oxidative damage and inflammation of the skin. Previous research has demonstrated that pilose antler extracts have strong anti-inflammatory properties and possess antioxidant effects. This study aimed to elucidate the mechanism of pilose antler protein in repairing photodamage caused by UVB radiation in HaCaT cells and ICR mice. Pilose antler protein (PAP) was found to increase the expression of type I collagen and hyaluronic acid in HaCaT cells under UVB irradiation while also inhibiting reactive oxygen species (ROS) production and oxidative stress in vitro. In vivo, the topical application of pilose antler protein effectively attenuated UVB-induced skin damage in ICR mice by reducing interleukin-1β (IL-β), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) and inhibiting skin inflammation while alleviating UVB-induced oxidative stress. It was shown that pilose antler protein repaired UVB-induced photodamage through the MAPK and TGF-β/Smad pathways. [ABSTRACT FROM AUTHOR]

To improve the utilization of by-products of the Hyriopsis cumingii, this study investigated the effect of Hyriopsis cumingii polysaccharide (HCP) on the proliferation and migration of normal cells, as well as its reparative effects on ultraviolet radiation-B (UVB)-damaged cells. First, HCP was isolated and purified using DEAE Cellulose-52 column chromatography, Sephadex G-100 column chromatography and nanofiltration. Then, structural analysis was conducted using high-performance liquid chromatography, high-performance gel permeation chromatography, and infrared spectroscopy. Following this, cell proliferation experiments, cell scratch tests, UVB damage experiments, and protein expression analyses were employed to explore the anti-UVB damage effects and corresponding mechanisms of polysaccharide components. The results indicated the three substances obtained by isolation and purification were all homogeneous polysaccharide components. Among them, HCP-2 played a major role in promoting cell proliferation in HCP and facilitated the migration of HaCaT cells. The recovery of UVB-damaged cell vitality was raised by the increasing concentration of HCP-2. Furthermore, the reparative effect was more substantial than the protective effect at the same sample concentration. It was also observed that HCP-2 up-regulated the expression of the anti-apoptotic protein bcl-2 while inhibited the expression of apoptosis-related proteins casp9, p-Akt, and p-p38, indicating that HCP-2 could repair HaCaT cells by regulating apoptosis of cells damaged by UVB. In conclusion, HCP had the ability to inhibit cell apoptosis which provide a theoretical basis for its future application in the development of food and health products.

This study investigated the effect of forkhead box M1 (FOXM1) and Aurora kinase B (AURKB) on the epidermal function of keratinocytes.

Ultraviolet-B (UVB) radiation is a major physical factor that induces structural changes in human skin. The aim of this study was to determine whether the novel silent information regulator 1 (sirtuin 1 SIRT1) protein activator, penilumamide, exerted any protective effects against UVB-induced skin damage using human HaCaT keratinocytes as a model. Enzymatic assays were performed to determine the SIRT1-activating ability of penilumamide, which was compared with that of resveratrol, a potent natural product SIRT1 activator with antioxidant and anti-inflammatory properties. Penilumamide markedly activated SIRT1 enzyme activity compared to resveratrol. To further investigate the protective effect of penilumamide against UVB-induced cytotoxicity, HaCaT cells were pretreated with penilumamide (10 μM) for 24 hr followed by irradiation with UVB (40 mJ/cm2). UVB (40 mJ/cm2) irradiation significantly reduced cell viability in a time-dependent manner, whereas pretreatment with penilumamide blocked this effect. Further, penilumamide decreased the levels of intracellular reactive oxygen species (ROS) generated by UVB irradiation in HaCaT cells. Pretreatment with penilumamide also prevented UVB irradiation-induced changes in mitochondrial membrane potential (ΔΨm). In addition, pretreatment with penilumamide significantly reduced the expression levels of pro-inflammatory cytokines, interleukin (IL)-6, IL-8, and IL-10 and phosphorylation of nuclear factor-kB (NF-kB). These results indicate that penilumamide protects HaCaT cells from UVB-induced inflammation. Taken together data demonstrate that penilumamide exerted protective effects against UVB-induced ROS generation in HaCaT cells. Therefore, penilumamide may be considered to be used as a new SIRT1 activator to protect human keratinocyte against UVB-induced damage. [ABSTRACT FROM AUTHOR]

Objective To investigate the effects of expression of microRNA-223（miR-223) on cell proliferation, cell cycle, apoptosis and inflammatory reaction of psoriasis and their mechanism. Methods Human immortalized keratinocytes HaCaT were cultured in vitro. The cells were divided into the control group, model group, model+miR-NC group, model+miR-223 inhibitor group. Except for the control group, cells in the other groups were induced to establish psoriasis cell models by M5 method. Real-time quantitative PCR （RT-qPCR） was used to detect the expression of miR-223 in each group. CCK-8 method and flow cytometry were used to detect cell proliferation activity, cell cycle, and apoptosis in each group. ELISA was used to detect the levels of inflammatory factors such as IL-6, IL-1β and TGF-β1 in supernatant. Western blotting was used to detect the expression of phosphatase and tensin homolog deleted on chromosome ten （PTEN) protein. Results Compared with the control group, the expression level of miR-223 significantly increased （P<0. 05), OD values at 48, 72 and 96 h and the proportion of cells in the cell cycle S phase significantly increased （all P<0. 05), the proportion of cells in the cell cycle G0/G1 and apoptosis rate significantly decreased （all P<0. 05), the levels of IL-6, IL-1β and TGF-β1 significantly increased (all P<0. 05), while the expression of PTEN protein decreased in the model group （P<0. 05）. Compared with the model +miR-NC group, the expression level of miR-223 inhibitor group significantly decreased （P<0. 05)，OD values at 48, 72 and 96 h and the proportion of cells in the S phase decreased （P<0. 05), the proportion of cells in the cell cycle G0/G1 and apoptosis rate significantly increased （P<0. 05), the levels of IL-6, IL-1β and TGF-β1 significantly decreased （P<0. 05), and PTEN protein expression increased in the model +miR-223 inhibitor group （P<0. 05）. There were no significant differences in the above indexes between the model group and the model +miR-NC group （all P>0. 05). Conclusions The expression level of miR-223 increases in psoriasis cells. Down-regulating the level of miR-223 can inhibit the proliferation and inflammatory response of psoriasis cells, and promote their apoptosis and block the cell cycle in G0/G1 phase， which may be related to its regulation of PTEN. [ABSTRACT FROM AUTHOR]

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

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

Keratinocytes, located in the outermost layer of human skin, are pivotal cells to resist environmental damage. Cellular autophagy plays a critical role in eliminating damaged organelles and maintaining skin cell homeostasis. Low‐dose 5‐Aminolevulinic acid photodynamic therapy (ALA‐PDT) has been demonstrated to enhance skin's antistress ability; however, the regulatory mechanisms of autophagy in keratinocytes remain unclear. In this study, we treated immortalized human keratinocytes (HaCaT cells) with low‐dose ALA‐PDT (0.5 mmol/L, 3 J/cm2). Through RNA‐sequencing analysis, we identified that low‐dose ALA‐PDT modulated autophagy‐related pathways in keratinocytes and pinpointed Unc‐51‐like kinase 1 (ULK1) as a key gene involved. Western blot results revealed that low‐dose ALA‐PDT treatment upregulated the expression of autophagy‐related proteins Beclin‐1 and LC3‐II/LC3‐I ratio. Notably, low‐dose ALA‐PDT regulated autophagy by inducing an appropriate level of reactive oxygen species (ROS), transiently reducing mitochondrial membrane potential, and decreasing adenosine triphosphate production; all these processes functioned on the AMP‐activated protein kinase (AMPK)/ULK1 pathway to activate autophagy. Finally, we simulated external environmental damage using ultraviolet B (UVB) at a dose of 60 mJ/cm2 and observed that low‐dose ALA‐PDT mitigated UVB‐induced cell apoptosis; however, this protective effect was reversed when using the autophagy inhibitor 3‐methyladenine. Overall, these findings highlight how low‐dose ALA‐PDT enhances antistress ability in HaCaT cells through controlling ROS generation and activating the AMPK/ULK1 pathway to arouse cellular autophagy. [ABSTRACT FROM AUTHOR]

Coffee pulp (CP), a by-product of coffee production, is an underutilized resource with significant potential value. CP contains monosaccharides that can serve as an ideal carbon source for bacterial cultivation, enabling the production of value-added components such as medical-grade cellulose. Herein, we extracted the sugar fraction from Arabica CP and used it as a supplement in a growing media of a bacteria cellulose (BC), Komagataeibacter nataicola. The BC was then characterized and tested for cytotoxicity. The CP sugar fraction yielded approximately 7% (w/w) and contained glucose at 4.52 mg/g extract and fructose at 7.34 mg/g extract. Supplementing the sugar fraction at different concentrations (0.1, 0.3, 0.5, 0.7, and 1 g/10 mL) in sterilized glucose yeast extract broth, the highest yield of cellulose (0.0020 g) occurred at 0.3 g/10 mL. It possessed similar physicochemical attributes to the BC using glucose, with some notable improvements in fine structure and arrangement of the functional groups. In cytotoxicity assessments on HaCaT keratinocyte cells, bacterial cellulose concentrations of 2–1000 µg/mL exhibited viability of ≥ 80%. However, higher concentrations were toxic. This research innovatively uses coffee pulp for bacterial cellulose, aligning with the principles of a bio-circular economy that focuses on sustainable biomass utilization. The sugar fraction of Arabica CP (6.64 g/100 g sample) contained glucose and fructose of 4.52 and 7.34 mg/g extract respectively. Different sugar fraction concentrations (0.1, 0.3, 0.5, 0.7, and 1 g/10 mL) were tested in sterilized glucose yeast extract broth. Optimal BC yield (0.0020 g) was achieved at 0.3 g/10 mL. The BC exhibited comparable physicochemical characteristics to cellulose obtained from glucose. The cytotoxicity indicate that HaCaT cells exposed to 2–1000 µg/mL of BC had a percentage cell viability of ≥80%, but it was toxic at higher concentrations. CP represents a cheap and readily-available source for BC production, contributing to the bio-circular economic goal. [ABSTRACT FROM AUTHOR]

Skin oxidative stress results in structural damage, leading to premature senescence, and pathological conditions such as inflammation and cancer. The plant‐derived prenylated pyrone–phloroglucinol heterodimer arzanol, isolated from Helichrysum italicum ssp. microphyllum (Willd.) Nyman aerial parts, exhibits anti‐inflammatory, anticancer, antimicrobial, and antioxidant activities. This study explored the arzanol protection against hydrogen peroxide (H2O2) induced oxidative damage in HaCaT human keratinocytes in terms of its ability to counteract cytotoxicity, reactive oxygen species (ROS) generation, apoptosis, and mitochondrial membrane depolarization. Arzanol safety on HaCaT cells was preliminarily examined by the 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide (MTT) assay and microscopic observation. The arzanol pre‐incubation (5–100 μM, for 24 h) did not induce cytotoxicity and morphological alterations. The phloroglucinol, at 50 μM, significantly protected keratinocytes against cytotoxicity induced by 2 h‐incubation with 2.5 and 5 mM H2O2, decreased cell ROS production induced by 1 h‐exposure to all tested H2O2 concentrations (0.5–5 mM), as determined by the 2′,7′‐dichlorodihydrofluorescein diacetate (H2DCFDA) assay, and lipid peroxidation (thiobarbituric acid reactive substances [TBARS] method). The 2‐h incubation of keratinocytes with H2O2 determined a significant increase of apoptotic cells versus control cells, evaluated by NucView® 488 assay, from the dose of 2.5 mM. Moreover, an evident mitochondrial membrane potential depolarization, monitored by fluorescent mitochondrial dye MitoView™ 633, was assessed at 5 mM H2O2. Arzanol pre‐treatment (50 μM) exerted a strong significant protective effect against apoptosis, preserving the mitochondrial membrane potential of HaCaT cells at the highest H2O2 concentrations. Our results validate arzanol as an antioxidant agent for the prevention/treatment of skin oxidative‐related disorders, qualifying its potential use for cosmeceutical and pharmaceutical applications. The 2 h‐exposure of human HaCaT keratinocytes to H2O2 induced cytotoxicity, morphological alterations, ROS production, apoptosis, and mitochondrial depolarization. Pre‐treatment (24 h) of keratinocytes with the phloroglucinol arzanol (50 μM), obtained from Helichrysum italicum ssp. microphyllum (Willd.) Nyman, preserved against H2O2‐induced oxidative damage. The phloroglucinol significantly protected keratinocytes against cytotoxicity induced by 2‐h incubation with 2.5 and 5 mM H2O2, decreased cell ROS production induced by 0.5–5 mM H2O2, and significantly reduced apoptotic cell number and mitochondrial membrane depolarization. [ABSTRACT FROM AUTHOR]

Background: Vitiligo, a prevalent hypopigmented skin disorder, profoundly impacts patients' psychological well-being and quality of life. Therefore, the development of more efficacious antivitiligo drugs is imperative. Objectives: The aim of this study was to investigate the protective effects of four flavonoids found in Vernonia anthelmintica (L.) Willd such as Butin, Butein, Eriodictyol, and Liquiritigenin—against H2O2-induced oxidative stress damage in human immortalized epidermal cells (HaCaT cells). Materials & Methods: Cytotoxicity was assessed using the MTT kit. Superoxide dismutase (SOD) activity was measured via the WST-1 method, while the content of malondialdehyde (MDA) was determined using the thiobarbituric acid method. Transcription and protein expression of nuclear transcription-related factors (Nrf2), heme oxidase-1 (HO-1), and Quinone oxidoreductase (NQO1) were analyzed through quantitative real-time polymerase chain reaction and Western Blotting. Results: Upon treatment with the four flavonoids, SOD activity exhibited a significant increase compared to the H2O2 induction model (P <.01), and MDA content was significantly lower (P <.01). This effect showed a dose-dependent relationship, with an increment in SOD activity and a reduction in MDA content. All four flavonoids upregulated the expression levels of nuclear transcription-related factor, HO-1, and NQO1 genes, as well as their corresponding proteins. Conclusion: The identified flavonoids in V anthelmintica (L.) Willd demonstrate a protective effect against H2O2-induced oxidative stress damage in HaCaT cells. [ABSTRACT FROM AUTHOR]

Copyright of Farmacia is the property of Societatea de Stiinte Farmaceutice Romania and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

This study aims to investigate the protective effects of the extract of Sophora japonica L. (Sophora extract) and vitamin C (VC) on UV-induced damage in HaCaT cells. HaCaT cells were cultured in vitro and divided into different groups: Control group (without UV irradiation or treatment with Sophora extract, VC, or their combination), UV radiation group, 125 μg/mL Sophora extract group (with UV irradiation and treatment with Sophora extract), 125 μg/mL vitamin C group (with UV irradiation and treatment with VC), and 125 μg/mL combination group (with UV irradiation, Sophora extract and VC at a mass ratio of 1:1). The inhibitory effects of Sophora extract, VC, and their combination on reactive oxygen species (ROS) production and mitochondrial ROS in UV-irradiated HaCaT cells were measured using fluorescence staining and enzyme-linked immunosorbent assay. Immunofluorescence staining and enzyme-linked immunosorbent assay were also employed to evaluate the expression levels of cyclobutane pyrimidine dimers (CPDs) and the inflammatory cytokine IL-6 in UV-irradiated HaCaT cells treated with Sophora extract, VC, or their combination. The results showed that the total ROS inhibition rates of Sophora extract, VC, and the combination in UVA-treated HaCaT cells were 38.23%±9.23%, 27.20%±6.87%, and 64.13%±4.08%, respectively. The combination significantly enhanced the total ROS inhibition rate compared to the individual treatments (P

Sunscreen products can protect the skin against the harmful effects of UV radiation, including reddening, aging, and cancer. The aim of this research was to evaluate the photoprotective effects of yeast pulcherrimin, an iron-chelating dipeptide. We first investigated the cytotoxicity of pulcherrimin produced by Metschnikowia pulcherrima yeast on the human keratinocyte HaCaT cell line, using the PrestoBlue assay. We assessed the ability of pulcherrimin to induce DNA repair after the exposure of HaCaT cells to oxidative stress. We also evaluated its protective activity against UVC radiation. The sun protective factor (SPF) was calculated using the Mansur equation. The UVA/UVB ratio values for pure pulcherrimin were evaluated using the Boots Star Rating system. The critical wavelength was determined by calculating the integrated optical density curve area. Based on the results, pulcherrimin shows strong cytoprotective effects through antioxidant and photoprotective activities on the HaCaT cell line. The calculated SPFs were 20 and 15 at pH = 7 and pH = 10, respectively. The critical wavelength above 370 nm and the UVA/UVB ratio R > 1 suggest that yeast pulcherrimin—a cyclic dipeptide containing iron—may be considered a promising photoprotective agent.

Abalone, a marine edible gastropod with nutritional value, is a popular seafood delicacy worldwide, especially in Asia; however, viscera by-products are generally discarded during processing. Therefore, we investigated the skin health benefits of abalone viscera ultrasonic extract (AVU) in human dermal fibroblasts (HDFs) and human keratinocyte (HaCaT) cells. AVU showed valuable protein contents, indicating that it is a worthy and safe material for industrial application. AVU increased collagen synthesis production and messenger RNA (mRNA) expression of Collagen Type I Alpha 1, 2, and 3 chains through the transforming growth factor beta/suppressor of mother against the decapentaplegic pathway in HDF cells. AVU also increased hyaluronic acid production, upregulated Hyaluronan Synthases 1, 2, and 3, filaggrin and aquaporin3 mRNA levels, and downregulated hyaluronidase mRNA levels in HaCaT cells. Furthermore, mechanistic studies showed that AVU increased the phosphorylation of extracellular signal-regulated kinase, p38, and cyclic AMP response-binding protein activation. AVU activated the transcription factors, phosphoinositide 3-kinase, protein kinase B, and nuclear factor kappa B cell p65 and downregulated the degranulation of inhibitory kappa B in HaCaT cells. Studies of hyaluronic acid production in AVU by inhibiting EKR, p38 and NF-κB have shown that p38 MAPK and NF-κB signaling are pivotal mechanisms, particularly in the AVU. These results demonstrated that AVU produced from by-products may improve skin health and may thus be used as a functional food and cosmetics ingredient.

The skin is constantly exposed to a variety of environmental threats. Therefore, the influence of environmental factors on skin damage has always been a matter of concern. This study aimed to investigate the cytotoxic effects of different environmental factors, including cooking oil fumes (COFs), haze (PM2.5), and cigarette smoke (CS), on epidermal HaCaT cells and dermal fibroblast (FB) cells. Cell viability, intracellular reactive oxygen species (ROS) generation, inflammatory cytokine levels, and collagen mRNA expression were used as toxicity endpoints. Additionally, the effects of ozone (O3) on cell viability and release of inflammatory cytokines in 3D epidermal cells were also examined. The results showed that the organic extracts of CS, COFs, and PM2.5 significantly inhibited the viability of HaCaT and FB cells at higher exposure concentrations. These extracts also increased intracellular ROS levels in FB cells. Furthermore, they significantly promoted the release of inflammatory cytokines, such as IL-1α and TNF-α, in HaCaT cells and down-regulated the mRNA expression of collagen I, III, IV, and VII in FB cells. Comparatively, SC organic extracts exhibited stronger cytotoxicity to skin cells compared to PM2.5 and COFs. Additionally, O3 at all test concentrations significantly inhibited the viability of 3D epidermal cells in a concentration-dependent manner and markedly increased the levels of TNF-α and IL-1α in 3D epidermal cells. These findings emphasize the potential cytotoxicity of COFs, PM2.5, CS, and O3 to skin cells, which may lead to skin damage; therefore, we should pay attention to these environmental factors and take appropriate measures to protect the skin from their harmful effects. [ABSTRACT FROM AUTHOR]

Deoxynivalenol (DON) is a mycotoxin frequently occurring in human and animal food worldwide, which raises increasing public health concerns. In the present study, we used human keratinocytes (HaCaT cells) as an in vitro model to explore the cytotoxic effect of DON. The results showed that the cells exhibited varying degrees of damage, including decreased cell number and viability, cell shrinkage and floating, when treated with 0.125, 0.25, and 0.5 μg/mL DON for 6, 12, and 24 h, respectively. Furthermore, exposure to DON for 24 h significantly increased the lactate dehydrogenase (LDH) release and intracellular reactive oxygen species (ROS), and prominently decreased the superoxide dismutase (SOD) and catalase (CAT) activity. Additionally, DON exposure induced mitochondrial damage and cell apoptosis through reducing mitochondrial membrane potential. Then, we performed RNA‐sequencing to investigate the molecular changes in HaCaT cells after DON exposure. The RNA‐sequencing results revealed that DON exposure altered the gene expression involved in apoptosis, MAPK signaling pathway, and PI3K/Akt signaling pathway. Moreover, DON exposure significantly decreased the mRNA and protein expression of Bcl‐2, and increased the mRNA and protein expression of Bax, Caspase 3 and COX‐2, the protein expression of PI3K, and the phosphorylation levels of Akt, ERK, p38, and JNK. Taken together, these findings suggest that DON exposure could induce cell damage, oxidative stress, and apoptosis in HaCaT cells through the activation of PI3K/Akt and MAPK pathways. [ABSTRACT FROM AUTHOR]

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

Extended exposure to UVB (280–315 nm) radiation results in oxidative damage and inflammation of the skin. Previous research has demonstrated that pilose antler extracts have strong anti-inflammatory properties and possess antioxidant effects. This study aimed to elucidate the mechanism of pilose antler protein in repairing photodamage caused by UVB radiation in HaCaT cells and ICR mice. Pilose antler protein (PAP) was found to increase the expression of type I collagen and hyaluronic acid in HaCaT cells under UVB irradiation while also inhibiting reactive oxygen species (ROS) production and oxidative stress in vitro. In vivo, the topical application of pilose antler protein effectively attenuated UVB-induced skin damage in ICR mice by reducing interleukin-1β (IL-β), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) and inhibiting skin inflammation while alleviating UVB-induced oxidative stress. It was shown that pilose antler protein repaired UVB-induced photodamage through the MAPK and TGF-β/Smad pathways.

Deoxynivalenol (DON) is a common mycotoxic contaminant, frequently found in food and feed, causing a severe threat to human and animal health. Because of the widespread contamination of DON, humans involved in agricultural practices may be directly exposed to DON through the skin route. Chlorogenic acid (CGA) is a phenolic acid, which has anti-inflammatory and antioxidant properties. However, it is still unclear whether CGA can protect against DON-induced skin damage. Here, the effect of CGA on mitigating damage to human keratinocytes (HaCaT) triggered by DON, as well as its underlying mechanisms were investigated. Results demonstrated that DON exposure significantly decreased cell viability, and induced excessive mitochondrial reactive oxygen species (mtROS) generation, mitochondrial damage, oxidative stress, cell apoptosis and pyroptosis. However, CGA pretreatment for 2 h significantly increased cell viability and reversed DON-induced oxidative stress by improving antioxidant enzyme activities such as superoxide dismutase (SOD), glutathione (GSH), catalase (CAT), reducing mtROS generation and enhancing mitochondrial function through activating Nrf2/HO-1 pathway. Moreover, CGA significantly increased the Bcl-2 protein expression, decreased the protein expressions of Bax and cleaved Caspase-3, and suppressed the phosphorylated of ERK, JNK, NF-κB. Further experiments revealed that CGA could also inhibit the pyroptosis-related protein expressions including NLRP3, cleaved Caspase-1, GSDMD-N, cleaved IL-1β and IL-18. In conclusion, our results suggest that CGA could attenuate DON-induced oxidative stress, inflammation, and apoptosis by activating the Nrf2/HO-1 pathway and inhibiting MAPK/NF-κB/NLRP3 pathway. CGA might be a novel promising therapeutic agent for alleviating the dermal damage triggered by DON.

The phytoconstituents of the aqueous extract from Syzygium jambos L. (Alston) leaves were defined using HPLC-PDA-MS/MS and the antioxidant, anti-aging, antibacterial, and anti-biofilm activities of the extract were in silico and in vitro investigated. The antioxidant activities were performed using in vitro DPPH and FRAP assays as well as H2-DCFDA assay in HaCaT cells in which oxidative stress was induced by UVA radiation. Anti-aging activity was tested in vitro, using aging-related enzymes. The antibacterial, anti-biofilm and inhibitory effects on bacterial mobilities (swarming and swimming) were assessed against Pseudomonas aeruginosa. Results showed that S. jambos aqueous extract contained 28 phytochemicals belonging to different metabolite classes, mainly phenolic acids, gallic acid derivatives, flavonoids, and ellagitannins. Mineral content analysis showed that S. jambos leaves contained moderate amounts of nitrogen, potassium, manganese, magnesium, and zinc, relatively low amounts of phosphorus and copper, and high concentration of calcium and iron. The extract displayed strong antioxidant activities in vitro and inhibited UVA-induced oxidative stress in HaCaT cells. Docking the major compounds identified in the extract into the four main protein targets involved in skin aging revealed an appreciable inhibitory potential of these compounds against tyrosinase, elastase, hyaluronidase, and collagenase enzymes. Moreover, molecular dynamic simulations were adopted to confirm the binding affinity of some selected compounds towards the target enzymes. The extract exhibited pronounced in vitro anti-aging effects, compared to kojic acid and quercetin (the reference compounds). It also inhibited the growth of P. aeruginosa, counteracted its ability to form biofilm, and impeded its swarming and swimming mobilities. Altogether, these findings strongly propose S. jambos leaves as a promising source of bioactive metabolites for the development of natural cosmeceutical and dermatological agents.

The skin is constantly exposed to a variety of environmental threats. Therefore, the influence of environmental factors on skin damage has always been a matter of concern. This study aimed to investigate the cytotoxic effects of different environmental factors, including cooking oil fumes (COFs), haze (PM2.5), and cigarette smoke (CS), on epidermal HaCaT cells and dermal fibroblast (FB) cells. Cell viability, intracellular reactive oxygen species (ROS) generation, inflammatory cytokine levels, and collagen mRNA expression were used as toxicity endpoints. Additionally, the effects of ozone (O3) on cell viability and release of inflammatory cytokines in 3D epidermal cells were also examined. The results showed that the organic extracts of CS, COFs, and PM2.5 significantly inhibited the viability of HaCaT and FB cells at higher exposure concentrations. These extracts also increased intracellular ROS levels in FB cells. Furthermore, they significantly promoted the release of inflammatory cytokines, such as IL-1α and TNF-α, in HaCaT cells and down-regulated the mRNA expression of collagen I, III, IV, and VII in FB cells. Comparatively, SC organic extracts exhibited stronger cytotoxicity to skin cells compared to PM2.5 and COFs. Additionally, O3 at all test concentrations significantly inhibited the viability of 3D epidermal cells in a concentration-dependent manner and markedly increased the levels of TNF-α and IL-1α in 3D epidermal cells. These findings emphasize the potential cytotoxicity of COFs, PM2.5, CS, and O3 to skin cells, which may lead to skin damage; therefore, we should pay attention to these environmental factors and take appropriate measures to protect the skin from their harmful effects.

Excessive UVB exposure increased the production of reactive oxygen species (ROS), leading to oxidative damage and epidermal inflammation. To enhance UVB protection effect, a strong phenolic antioxidant, ferulic acid (FA) was designed onto HA via a free radical mediated method. Our previous work has confirmed its structural characterization and in vitro antioxidant. The aim of this study was to evaluate its protective effects against UVB-induced damage in human HaCaT cells. We observed a significant reduction in cell viability to 57.43 % following UVB exposure at a dose of 80 mJ/cm2. However, pretreatment with FA-HA (250 to 2000 μg·mL−1) significantly attenuated cytotoxicity in a dose-dependent manner. Furthermore, FA-HA was found to suppress the intracellular generation of ROS and up-regulated the expression of the antioxidant enzyme superoxide dismutase (SOD). The elevated levels of pro-inflammatory cytokines, including interleukin-1 beta (IL-1β), interleukin-6 (IL-6), interleukin-8 (IL-8) and tumor necrosis factor-alpha (TNF-α) as well as the mRNA expression of matrix metalloproteinase-1/9 (MMP-1/9) induced by UVB irradiation, were also effectively reduced by FA-HA. Additionally, FA-HA treatment decreases the phosphorylation of mitogen-activated protein kinase (MAPK) and activator protein-1 (AP-1), ultimately preventing apoptosis. These findings suggest that FA-HA is a promising candidate for UVB protection in skincare formulations. [ABSTRACT FROM AUTHOR]

Psoriasis, a widespread skin condition impacting over 100 million individuals globally, is characterised by uncontrolled hyperproliferation of keratinocytes, abnormal apoptosis, and excessive secretion of inflammatory cytokines and angiogenic factors. Traditional use of Alstonia scholaris (L.) R.Br. , Wrightia tinctoria (Roxb.) R.Br. and Solanum xanthocarpum Schrad. & Wendl. in Ayurveda and Siddha medicinal systems have shown promising anti-inflammatory and wound-healing properties. However, underlying mechanisms of their phytoactivity in addressing psoriasis-like skin inflammation on human keratinocytes remain largely unexplored. The study was aimed to investigate anti-psoriatic potential of ethyl acetate and ethanolic extracts of A. scholaris, W. tinctoria and S. xanthocarpum in human keratinocyte cell line (HaCaT). Ethyl acetate and ethanolic extracts of A. scholaris (ASEA and ASE), W. tinctoria (WTEA and WTE) and S. xanthocarpum (SXEA and SXE) were first subjected to phytochemical screening through high-performance liquid chromatography (HPLC) using their marker compound loganin, kaempferol and chlorogenic acid, respectively. The proliferation inhibition efficiency of these extracts was measured using MTT assay on HaCaT cell line. Subsequently, the apoptotic effect of these extracts on HaCaT cell line was determined by JC-1 and Annexin V assays. Furthermore, IL-8 and RANTES levels were measured in TNF-alpha-induced HaCaT cell line post-treatment with these extracts to determine their anti-inflammatory properties. ASEA, ASE, WTEA, WTE, SXEA and SXE significantly inhibited proliferation of keratinocytes (HaCaT cells) and resulted in the induction of apoptotic markers (mitochondrial membrane potential and phosphatidyl serine externalization). Additionally, pro-inflammatory markers (IL-8 and RANTES levels) were downregulated in HaCaT cells. The anti-proliferative effects were particularly distinct at higher concentrations (200 μg/mL), with inhibition rates reaching over 85% for W. tinctoria and S. xanthocarpum extracts. In apoptotic assays, notable increases in late apoptotic or necrotic cell populations and significant losses in mitochondrial membrane potential were observed. All extracts markedly reduced the secretion of inflammatory mediators IL-8 and RANTES. All three plants exerted an anti-psoriatic effect at the cellular level via multiple parameters (anti-proliferative, pro-apoptotic, anti-inflammatory effect). This study provides insight into the mechanism of action of ASEA, ASE, WTEA, WTE, SXEA and SXE and highlights their promising potential for development as herbal therapeutic agents for psoriasis. It emphasizes the need for further pharmacological evaluation and toxicological studies of these extracts. [Display omitted] [ABSTRACT FROM AUTHOR]

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. [Display omitted] [ABSTRACT FROM AUTHOR]

A large portion of neuropathic pain suffering patients may also concurrently experience neuropathic itch, with a negative impact on the quality of life. The limited understanding of neuropathic itch and the low efficacy of current anti-itch therapies dictate the urgent need of a better comprehension of molecular mechanisms involved and development of relevant animal models. This study was aimed to characterize the itching phenotype in a model of trauma-induced peripheral neuropathy, the spared nerve injury (SNI), and the molecular events underlying the overlap with the nociceptive behavior. SNI mice developed hyperknesis and spontaneous itch 7-14 days after surgery that was prevented by gabapentin treatment. Itch was associated with pain hypersensitivity, loss of intraepidermal nerve fiber (IENF) density and increased epidermal thickness. In coincidence with the peak of scratching behavior, SNI mice showed a spinal overexpression of IBA1 and GFAP, microglia and astrocyte markers respectively. An increase of the itch neuropeptide B-type natriuretic peptide (BNP) in NeuN+ cells, of its downstream effector interleukin 17 (IL17) along with increased pERK1/2 levels occurred in the spinal cord dorsal horn and DRG. A raise in BNP and IL17 was also detected at skin level. Stimulation of HaCat cells with conditioned medium from BV2-stimulated SH-SY5Y cells produced a dramatic reduction of HaCat cell viability. This study showed that SNI mice might represent a model for neuropathic itch and pain. Collectively, our finding suggest that neuropathic itch might initiate at spinal level, then affecting skin epidermis events, through a glia-mediated neuroinflammation-evoked BNP/IL17 mechanism., Competing Interests: Declaration of competing interest The authors have no conflicts of interest to declare., (Copyright © 2024 The Authors. Published by Elsevier Ltd.. All rights reserved.)

Eukaryotic translation initiation factor 6 (eIF6) plays a crucial role in 60S ribosome biogenesis and protein translation, as well as in hypertrophic scar formation, but its potential role in epithelialization is still poorly understood. Herein, we found that eIF6 negatively correlated with the wound healing process. Mice with genetically knockdown eIF6 (eIF6+/-) showed faster re-epithelization as shown by the longer tongue of the newly formed epidermis. Furthermore, eIF6 ablation accelerated the wound healing process by targeting basal keratinocytes in the eIF6 keratinocyte-conditional knockout (eIF6f/+; Krt5-Cre+) mice. Mechanistically, keratin 6B, an important wound-activated protein, was significantly upregulated in eIF6f/+; Krt5-Cre+ mice skin as proved by RNA-seq, western immunoblots, and immunofluorescence staining. Moreover, an elevated level of KRT6B and accelerated proliferative capacity were also observed in stable knockdown eIF6 HaCaT cells. Taken together, eIF6 downregulation could accelerate epithelialization by upregulating KRT6B expression and promoting keratinocyte proliferation. Our results for the first time indicate that eIF6 might be a novel target to regulate re-epithelialization., (© The Author(s) 2024. Published by Oxford University Press.)

Background: Broussonetia papyrifera (L.) L'Hér. ex Vent (B. papyrifera) is a deciduous tree widely distributed in Asia. Previous studies have revealed that leaves of B. papyrifera ameliorated atopic dermatitis (AD)-like symptoms and inflammatory response. However, the impact and underlying mechanism of other parts of B. papyrifera on AD remain elusive., Methods: The AD mice induced by 1-Chloro-2,4-dinitrochlorobenzene were used to observe the histopathological alterations in the skin tissues using hematoxylin-eosin staining and toluidine blue staining techniques. Serum levels of inflammatory factors were quantified utilizing ELISA. Pyroptosis was analyzed by lactate dehydrogenase release and flow cytometry in human keratinocytes. The activation of Nod-like receptor protein 3 (NLRP3) inflammasome was analyzed by western blots. Furthermore, the mechanism underlying the inhibition of NLRP3 inflammasome by N-butanol extracts of B. papyrifera root bark (NE-BPRB) was investigated using cellular thermal shift assay and surface plasmon resonance techniques., Results: Treatment with NE-BPRB significantly ameliorated symptoms of AD mice and reduced serum levels of pro-inflammatory factors. NE-BPRB intervention exhibited inhibitory effects on NLRP3 inflammasome activation and pyroptosis in vitro and in vivo. NE-BPRB and its primary bioactive constituent chlorogenic acid (CA) promote the K48-linked ubiquitination of NLRP3, leading to its proteasomal degradation by binding WW domain containing E3 ubiquitin protein ligase 1 (WWP1)., Conclusions: The NE-BPRB and its primary bioactive constituent, CA, effectively inhibit the formation of the NLRP3 inflammasome and impede cell pyroptosis by promoting K48-linked ubiquitin-dependent proteasomal degradation of NLRP3 through binding to the E3 ubiquitin ligase WWP1, thereby resulting in improved AD., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 The Authors. Published by Elsevier Masson SAS.. All rights reserved.)

Background: Butin is a naturally occurring compound with a wide range of medicinal properties, including anti-inflammatory, anti-arthritic, and antioxidant properties. Particulate matter 2.5 (PM 2.5 ) and ultraviolet B (UVB) radiation contribute to skin cell damage via the induction of oxidative stress., Methods: This study sought to assess the protective effects of butin against damage triggered by PM 2.5 and UVB in human HaCaT keratinocytes. Assessments were performed to evaluate cell viability, apoptosis, and cellular component damage., Results: Butin exhibited its protective ability via the inhibition of PM 2.5 -induced reactive oxygen species generation, lipid peroxidation, DNA damage, protein carbonylation, and mitochondrial damage. Butin reduced the PM 2.5 -induced c-Fos and phospho-c-Jun protein levels as well as mitogen-activated protein kinase. Furthermore, butin mitigated PM 2.5 - and UVB-induced apoptosis., Conclusion: Butin had the potential as a pharmaceutical candidate for treating skin damage caused by PM 2.5 and UVB exposure., (© 2024 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

Despite substantial advancements in wound dressing development, effective skin repair remains a significant challenge, largely due to the persistent issue of recurrent infections. Three-dimensional printed constructs that integrate bioactive and antibacterial agents hold significant potential to address this challenge. In this study, a 3D-printed hydrogel scaffold composed of polyallylamine hydrochloride (PAH) and pectin (Pc), incorporated with mupirocin (Mp)-loaded quaternized chitosan nanoparticles (QC NPs) was fabricated. The primary objective of this study was to facilitate a controlled and sustained release of Mp via the QC NPs. The average size of QC-Mp nanoparticles was measured to be 66.05 nm and the average strand diameter and pore size of the 3D-printed construct were measured as 147.22 ± 5.83 and 388.44 ± 14.50 μm, respectively. The hemolysis rate of all scaffolds was below 2 %, indicating that they can be classified as non-hemolytic materials with sufficient blood compatibility. The PAH-Pc/QC-Mp scaffold exhibited significant antibacterial activity, enhanced cell viability in HaCat cells, sustained Mp release until day 7 (⁓60 %), and in-vivo wound healing promotion by stimulation of human keratinocytes. In conclusion, the proposed biocompatible construct demonstrates significant potential for the treatment of chronic and infected wounds by preventing infection and promoting accelerated wound healing., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier B.V. All rights reserved.)

Arsenic, a widespread environmental contaminant, is highly toxic to human health. Arsenic exposure is associated with the occurrence of skin lesions and diseases. This study investigated the dermal toxicity of trivalent arsenicals (As III and MMA III ) and its underlying mechanism using human keratinocyte cell line and ex vivo porcine skin. As III and MMA III induced concentration-dependent cell apoptosis and necrosis in HaCaT cells, which was confirmed in ex vivo porcine skin. As III and MMA III increased reactive oxygen species generation and GSH depletion. Interestingly, radical scavenger antioxidants such as Vitamin C failed to mitigate arsenic-induced cytotoxicity, while thiol-containing compounds effectively alleviated it, suggesting a key role of thiol depletion in the trivalent arsenical-induced dermal toxicity. DMSA showed the strongest protective effects against As III and MMA III -induced cytotoxicity in HaCaT cells. Of note, DMSA restored arsenical-induced tissue damage, and reduced the apoptosis in ex vivo porcine skin, highlighting its potential use to alleviate arsenic-induced skin lesions and diseases., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier Inc. All rights reserved.)

The active ingredients of plants were screened by molecular docking technology and the result were verified. According to the verification results of molecular docking, the five active ingredients were combined in equal proportions to form a compound drug. In the HaCaT photoaging model, the effects of the compound drug on antioxidant and senescence-associated secretory phenotype (SASP) factors of the NF-κB and MAPK pathways were studied via SOD and MDA kits, DCFH-DA fluorescent probes and ELISA. In the skin photoaging model, the effects of the compound drug on antioxidants and the SASP factors of the NF-κB and MAPK pathways were studied via SOD, MDA, and CAT kits and ELISA. The results revealed that the compound drug increased SOD activity, decreased the MDA content and intracellular ROS, inhibited IL-6 in the NF-κB pathway, and inhibited MMP-1 and collagen I in the MAPK pathway. The results of HE, Masson and Victoria blue skin staining revealed that the compound drug inhibited abnormal thickening of the epidermis, abnormal breaking and accumulation of collagen fibers and elastic fibers, and maintained their orderly arrangement. Moreover, the results revealed that the compound drug increased SOD, CAT and collagen I, and reduced the MDA content, the SASP factors IL-6 and TNF-α of the NF-κB pathway, and the SASP factors MMP-1 of the MAPK pathway. The above results indicate that the active ingredients of the compound drug screened by molecular docking have the potential to reduce skin photoaging., (© 2024. The Author(s), under exclusive licence to Springer Nature B.V.)

Background: The intestinal and skin epithelium play a strong role against bacterial stimuli which leads to inflammation and oxidative stress when overwhelmed. Polyphenols from fruit-rich diets and by-products show promise against bacterial deleterious effects; however, their antibacterial and health-promoting effects remain understudied., Purpose: This study aimed to assess the impact of polyphenolic extracts of grape (GrPE), persimmon (PePE) and pomegranate (PoPE) by-products on bacterial pathogen-host interactions, focusing beyond growth inhibition to explore their effects on bacterial adhesion, invasion, and modulation of host responses., Methods: The microdilution method, as well as the tetrazolium based MTT cell proliferation and cytotoxicity assay with crystal violet staining were used to identify extracts sub-inhibitory concentrations that interfere with bacterial adhesion, invasion or lipopolysaccharides (LPS) effect on cell hosts without compromising host viability. The cytoprotective effects of extracts were assessed in a knock-down model of nuclear factor erythroid 2-related factor 2 (Nrf2)., Results: All extracts demonstrated significant reductions in pathogen adhesion to Caco-2 and HaCaT cells while preserving cellular integrity. Notably, PePE exhibited specific efficacy against Salmonella enterica adhesion, attributed mostly to its gallic acid content, whereas PoPE reduced S. enterica invasion in Caco-2 cells. The extracts supported the prevalence of non-pathogenic and commensal strains of intestinal and skin surfaces, selectively reducing pathogenic adhesion. The extracts mitigated the oxidative stress, enhanced the barrier function, and modulated the pro-inflammatory cytokines in LPS-challenged cells. GrPE, rich in anthocyanins, and PePE were found to mediate their protective effects through Nrf2 activation, while PoPE exerted multifaceted actions independent of Nrf2., Conclusion: Our results highlight the therapeutic potential of GrPE, PePE, and PoPE in shaping bacterial-host interactions, endorsing their utility as novel nutraceuticals for both oral and topical applications to prevent potential bacterial infections through innovative mechanisms., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Crown Copyright © 2024. Published by Elsevier GmbH. All rights reserved.)

Psoriasis is a chronic inflammatory skin condition with numerous causes, including genetic, immunological and infectious factors. The course of psoriasis is long and recurrence is common; pathogenesis is not completely understood. However, there is an association between advancement of psoriasis and aberrant microRNA (miR or miRNA)‑155 expression. Through bioinformatics, the present study aimed to analyze the differentially expressed genes and miRNAs in psoriasis and its biological mechanism and function psoriatic inflammation. First of all, differentially expressed genes (DEGs) and miRNAs (DEMs) in patients with psoriasis were identified using GEO2R interactive web application. A psoriasis inflammatory model was established using lipopolysaccharide (LPS)‑treated HaCaT keratinocytes, which were transfected with miR‑155 mimic or inhibitor. Cell Counting Kit‑8 was used for the assessment of cell viability and proliferation, and changes in the cell cycle were examined using flow cytometry. ELISA and reverse transcription‑quantitative PCR (RT‑qPCR) were used to detect the expression levels of the inflammatory factors IL‑1β and IL‑6. The dual‑luciferase reporter assay was used to verify the targeting association between miR‑155‑5p and IFN regulatory factor 2 binding protein 2 (IRF2BP2). To verify the targeting association of miR‑155 and the IRF2BP2/kruppel‑like factor 2 (KLF2)/NF‑κB signaling pathway, expression levels of IRF2BP2, KLF2 and p65 were identified by RT‑qPCR and western blotting. IRF2BP2 levels were also confirmed by immunofluorescence, in conjunction with bioinformatics database analysis. Overexpression of miR‑155 inhibited proliferation of HaCaT cells and increased the number of cells in S phase and decreasing number of cells in G1 and G2 phase. In the LPS‑induced inflammatory state, miR‑155 overexpression heightened the inflammatory response of HaCaT cells while inhibition of miR‑155 lessened it. Suppression of inflammatory cytokine expression by miR‑155‑5p inhibitor was reversed by knockdown of IRF2BP2. miR‑155 was shown to interact with IRF2BP2 to negatively regulate its expression, leading to decreased KLF2 expression and increased p65 expression and secretion of inflammatory factors, intensifying the inflammatory response of HaCaT cells. Therefore, miR‑155 may contribute to development of psoriasis by inducing tissue and cell damage by increasing the inflammatory response of HaCaT cells via the IRF2BP2/KLF2/NF‑κB pathway. In conclusion, the results of the present study offer novel perspectives on the role of miR‑155 in the onset and progression of psoriasis.

Background: Psoriasis (PSO) poses a global health threat. The current research challenge in PSO is relapse. Liquiritin (LIQ), a major active compound from Glycyrrhiza inflata Batalin, has multiple pharmacological properties, including anti-inflammatory and anti-proliferative. Nonetheless, the precise mechanisms underlying LIQ's therapeutic actions in PSO and prevention abilities remain elusive., Purpose: The present study aimed to delve into the potential to treat and prevent PSO and the mechanism of LIQ., Methods: The anti-inflammatory and anti-proliferative effects of LIQ were studied in vitro with the HaCaT cell line. Then, Transcriptional analysis and bioinformatic analysis were used to determine the internal associations of the target set. Subsequently, functional experiment, luciferase report assay, ChIP-PCR, and immunohistochemical validation of clinical samples were performed to investigate the mechanism of LIQ. Finally, the anti-psoriatic effects and prevention abilities of LIQ were verified in vivo with imiquimod (IMQ)-induced PSO-like mouse models., Results: Here, we identified differentially expressed genes in LIQ-stimulated HaCaT cells and Retinol-Binding Protein 3 (RBP3) as the core target, whereas YY1 was a predicted upstream transcription factor of RBP3. The YY1/RBP3 axis was obviously altered after administering LIQ at optimal doses of 20 μM in vitro and 100 µg/ml in vivo. LIQ can significantly inhibit the progression of PSO in vivo. Notably, LIQ also prevented the relapse of psoriatic lesions induced by the second round of low-dose IMQ. Mechanistically, we observed that LIQ could increase the promotion of YY1 for RBP3 by enhancing the binding affinity between them., Conclusion: These findings revealed that the YY1/RBP3 axis is a potential psoriatic target, and LIQ is a promising and innovative therapeutic candidate for the treatment and prevention of PSO., Competing Interests: Declaration of competing interest The authors declare that there are no conflicts of interest., (Copyright © 2024 Elsevier GmbH. All rights reserved.)

Patients suffering from diabetes mellitus are prone to develop diabetic wounds that are non-treatable with conventional therapies. Hence, there is an urgent need of hour to develop the therapy that will overcome the lacunas of conventional therapies. This investigation reports the Quality by Design-guided one-pot green synthesis of unique Opto-Laser activatable nanoSilver ThermoGel (OL→nSil-ThermoGel) for hyperthermia-assisted treatment of full-thickness diabetic wounds in mice models. The characterization findings confirmed the formation of spherical-shaped nanometric Opto-Laser activatable nanoSilver (30.75 ± 2.7 nm; ∆T: 37 ± 0.2 °C → 66.2 ± 0.1 °C; at 1.8 W/cm 2 NIR laser density). The findings indicated acceptable in vitro cytocompatibility and significant keratinocyte migration (95.04 ± 0.07 %) activity of OL→nSil towards HaCaT cells. The rheological data of OL→nSil hybridized in situ thermoresponsive gel (OL→nSil-ThermoGel) showed the gelling temperature at 32 ± 2 °C. In vivo studies on full-thickness diabetic wounds in a Mouse model showed OL→nSil-ThermoGel accelerated wound closure (94.42 ± 1.03 %) and increased collagen synthesis, angiogenesis, and decreased inflammatory markers. Similarly, immunohistochemistry study showed significant angiogenesis and faster phenotypic switching of fibroblasts to myofibroblasts in OL→nSil-ThermoGel treated diabetic wounds. Histological evaluation revealed a marked rise in keratinocyte migration, organized collagen deposition, and early regeneration of the epithelial layer compared to the diabetic wound control. In conclusion, the OL→nSil-ThermoGel modulates the cytokines, re-epithelialization, protein expression, and growth factors, thereby improving the repair and regeneration of diabetic wounds in mice., Competing Interests: Declaration of competing interest The authors declare the conflict of interest. The work described in this manuscript has been filed for an Indian patent at the Indian Patent Office (IPO), Mumbai, India; Application No.: 202321049846; Date of Application: 24/07/2023., (Copyright © 2024 Elsevier B.V. All rights reserved.)

Thirty-four phytochemicals were isolated from dry tubers of Bletilla striata Rchb.f. The compounds were classified as bibenzyls 1 - 14 , dihydrophenanthrenes 15 , 17 , 20 , 21 , phenanthrenes 16 , 18 , 19 , simple benzoids 22 - 24 , a fatty acid 25 , glucosyloxybenzyl 2-isobutylmalates 26 - 32 , and glucosyloxybenzyl cinnamates 33 , 34 . Compounds 1 - 4 , 7 , 8 , 11 , 12 , and 16 inhibited melanogenesis (17.96-55.27%) induced by α-MSH in B16F10 cells at 10-40 μM. However, compounds 9 , 10 , 17 , 18 , and 21 exhibited significant cytotoxicity against melanomas, with IC 50 values of 12-34 μM. Additionally, compounds 15 , 17 , 19 , 20 , 23 , 31 , and 33 reduced the ROS generation induced by H 2 O 2 in HaCaT cells at 6.25-100 μM. In particular, compounds 15 , 19 , and 20 strongly inhibited ROS generation, with IC 50 values of 2.15-9.48 μM. Consequently, compounds 1 - 4 , 7 - 12 , and 15 - 21 may be the strongest leads to follow in B. striata extract for further research on the skin disorders, hyperpigmentation, melanoma, and ageing.

Atopic dermatitis (AD), a chronic inflammatory disease, severely interferes with patient life. Human placenta extract (HPH; also known as human placenta hydrolysate) is a rich source of various bioactive substances and has widely been used to dampen inflammation, improve fatigue, exert anti-aging effects, and promote wound healing. However, information regarding HPH's incorporation in AD therapies is limited. Therefore, this study aimed to evaluate HPH's effective potential in treating AD using tumor necrosis factor (TNF)-α/interferon (IFN)-γ-stimulated human keratinocytes (HaCaT), immunized splenocytes, and a 2,4-dinitrochlorobenzene (DNCB)-induced AD mouse model. In TNF-α /IFN-γ-stimulated HaCaT cells, HPH markedly reduced the production of reactive oxygen species (ROS) and restored the expression of nuclear factor erythroid 2-related factor 2 (Nrf2), superoxide dismutase 1(SOD1), catalase, and filaggrin (FLG). HPH reduced interleukin (IL)-6; thymus- and activation-regulated chemokine (TARC); thymic stromal lymphopoietin (TSLP); and regulated upon activation, normal T cell expressed and presumably secreted (RANTES) levels and inhibited nuclear factor kappa B phosphorylation. Additionally, HPH suppressed the T helper 2 (Th2) immune response in immunized splenocytes. In the AD-like mouse model, it significantly mitigated the DNCB-induced elevation in infiltrating mast cells and macrophages, epidermal thickness, and AD symptoms. HPH also reduced TSLP levels and prevented FLG downregulation. Furthermore, it decreased the expression levels of IL-4, IL-5, IL-13, TARC, RANTES, and immunoglobulin E (IgE) in serum and AD-like skin lesion. Overall, our findings demonstrate that HPH effectively inhibits AD development and is a potentially useful therapeutic agent for AD-like skin disease.

Ethnopharmacological Relevance: Ecliptea herba, a traditional Chinese herbal medicine for hair loss, was first recorded in the Tang Dynasty's 'Qian Jin Yue Ling', of which the active ingredients and mechanisms of action in the treatment of chemotherapy-induced hair loss remain poorly investigated., Aim of the Study: To investigate the effects of the petroleum ether extract of Eclipta (PEE) on alopecia and follicle damage and elucidate its potential therapeutic mechanisms using the integration of network pharmacology, bioinformatics, and experimental validation., Materials and Methods: UPLC-MS was used to analyse the chemical composition of PEE. A network pharmacology approach was employed to establish the 'components-targets-pathways' network of PEE to explore potential therapeutic pathways and targets. Molecular docking was used for validation, and the mechanism of PEE in treating chemotherapy-induced alopecia (CIA) was elucidated using in vitro and in vivo on CIA models., Results: UPLC-MS analysis of PEE revealed 185 components, while network pharmacology and molecular docking analyses revealed potential active compounds and their target molecules, suggesting the involvement of core genes, such as TP53, ESR1, AKT1, IL6, TNF, and EGFR. The key components included wedelolactone, dimethyl-wedelolactone, luteoloside, linarin, and hispidulin. In vivo, PEE promoted hair growth, restored the number of hair follicles, and reduced follicle apoptosis. Conversely, in vitro, PEE enhanced cell viability, reduced apoptosis, and protected HaCaT cells from damage induced by 4-hydroperoxycyclophosphamide (4-HC)., Conclusions: PEE alleviated hair follicle damage in CIA mice by inhibiting the P53/Fas pathway, which may be associated with inhibiting hair follicle cell apoptosis. This study provides a novel therapeutic strategy for treating cyclophosphamide-induced hair loss., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier B.V. All rights reserved.)

Currently, LCCP is widely present in environmental media as well as animal and human samples, suggesting that exposure to LCCP may have posed a threat to the health of animals and humans. Skin is one of the important pathways for LCCP exposure. To clarify the effects of LCCP exposure on the skin, we have utilized two skin cell models, HaCaT and L929, to investigate the complex impacts of LCCP exposure on skin cell senescence and its potential regulatory mechanism(s). Firstly, the expression of senescence-related markers, including SA-β-Gal staining, p16, p21, and p53 proteins, were evaluated, and the results showed that skin cell senescence occurred under the treatment of LCCP. Moreover, our findings revealed that LCCP exposure triggered the activation of the NF-κB signaling pathway, prompting an inflammatory response in skin cells. To further understand the potential molecular mechanism of skin cell senescence induced by LCCP, according to our preliminary experimental results, we hypothesized that mtROS and Ca 2+ might have played an important role in the LCCP-induced senescence of skin cells. Based on this hypothesis, the use of mtROS and Ca 2+ inhibitors revealed a reduction in LCCP-triggered cell senescence and oxidative stress, validating our speculation. Similarly, in vivo experiments showed that LCCP enhanced the expression of inflammatory factors in mouse skin tissue, inhibiting skin proliferation and collagen level. This discovery was consistent with the findings from in vitro experiments. In summary, our experiments emphasized that both in vitro and in vivo, exposure to LCCP could induce skin aging, potentially through oxidative stress mediated by Ca 2+ overload, leading to skin aging damage. The research presented here establishes an important foundation for continued examination of the toxicology characteristics of LCCP., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier B.V. All rights reserved.)

Background: High glucose level and chronic inflammation are characteristic features of diabetic cutaneous wounds. Keratinocytes make up the epidermis and play an important role in skin repair. However, metabolomic changes of keratinocytes in chronic diabetic ulcers have not been fully studied., Methods and Results: This study used high levels of glucose combined with lipopolysaccharide to treat human HaCaT keratinocytes. Untargeted metabolomic combined with colorimetric assays were used to explore the changes of keratinocyte metabolites and related metabolic pathways caused by high glucose and lipopolysaccharide. Results demonstrated that high glucose combined with lipopolysaccharide treatment increased intracellular reactive oxygen species and impaired proliferation and migration of keratinocytes. Untargeted metabolomics analysis identified a total of 273 differential metabolites. Redox metabolism associated metabolites were largely altered. Reduced nicotinamide adenine dinucleotide, gamma-glutamylcysteine, superoxide dismutase activity and SOD2 gene expression were significantly upregulated while nicotinamide adenine dinucleotide, glutathione, glutathione peroxidase, several types of lysophosphatidylcholine, lysophosphatidylinositol, and GPR55 gene expression were downregulated. Alterations of glutathione and nicotinamide adenine dinucleotide were verified by colorimetric assays. For the first time, high glucose and LPS were observed to boost the levels of fructose, aldose reductase and sorbitol dehydrogenase of the polyol pathway in HaCaT cells. Further treatment of HaCaT with fructose leading to inhibition of cell proliferation and migration., Conclusions: Our data suggest high glucose combined with lipopolysaccharide significantly altered redox homeostasis associated metabolites and activate the polyol pathway in keratinocytes to impact cell proliferation and migration, providing new strategies for the treatment of chronic diabetic ulcers., (© 2024. The Author(s), under exclusive licence to Springer Nature B.V.)

The skin acts as a vital barrier, shielding the body from external threats that can trigger dryness, itching, and inflammation. Pilea mongolica, a traditional Chinese medicinal herb, holds promise for various ailments, yet its anti-inflammatory properties remain understudied. This study aimed to explore the potential anti-inflammatory effects of the methanol extract of P. mongolica (MEPM) and its underlying molecular mechanisms and active compounds in LPS-stimulated human keratinocytes. MEPM treatment, at concentrations without cytotoxicity, significantly decreased NO productions and the iNOS, IL-6, IL-1β, and TNF-α levels in LPS-induced HaCaT cells. Moreover, MEPM suppressed IRAK4 expression and phosphorylation of JNK, ERK, p38, p65, and c-Jun, suggesting that the anti-inflammatory effects of MEPM result from the inhibition of IRAK4/MAPK/NF-κB/AP-1 signaling pathway. Through LC/MS/MS analysis, 30 compounds and 24 compounds were estimated in negative and positive modes, respectively, including various anti-inflammatory compounds, such as corilagin and geraniin. Through HPLC analysis, geraniin was found to be present in MEPM at a concentration of 18.87 mg/g. Similar to MEPM, geraniin reduced iNOS mRNA expression and inhibited NO synthesis. It also decreased mRNA and protein levels of inflammatory cytokines, including IL-6 and TNF-α, and inhibited IRAK4 expression and the phosphorylation of MAPKs, NF-κB, and AP-1 pathways. Therefore, it can be inferred that the anti-inflammatory effects of MEPM are attributable to geraniin. Thus, MEPM and its active compound geraniin are potential candidates for use in natural functional cosmetics., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier B.V. All rights reserved.)

This study presents a comprehensive analysis of IFN-γ-Gaillardin nanoparticles (NPs) using a combination of computational, biophysical and cell-based approaches. The molecular docking analysis revealed that both hydrogen and hydrophobic forces are involved in the formation of IFN-γ-Gaillardin complex The interaction between IFN-γ and Gaillardin was further characterized by a pronounced ANS fluorescence spectrum peak and a higher intensity for IFN-γ. The Langmuir, Scatchard, and Hill analyses revealed a higher affinity and lower dissociation constant for IFN-γ NPs compared to IFN-γ alone, suggesting enhanced complex stability. Thermal gravimetric analysis confirmed that the Gaillardin interaction might improve the thermal stability of the NPs. The NPs demonstrated robust stability in various media, highlighting their potential as a delivery system. However, size increase in deionized water suggests the need for formulation optimization. Cell-based assays revealed selective cytotoxicity towards A-375 melanoma cancer cells with minimal impact on non-cancerous HaCaT cells, indicating targeted antitumor effects. Real-time PCR showed gene expression changes consistent with antitumor activity and immune response modulation. The findings suggest that IFN-γ-Gaillardin NPs have potent antitumor properties and the ability to modulate the immune system, warranting further investigation into their therapeutic applications. The development of an IFN-γ-based nanocarrier system for Gaillardin delivery offers a promising approach to melanoma therapy, setting a new direction for NP-based cancer treatment strategies., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024. Published by Elsevier B.V.)

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.

The influence of UV radiation on skin discoloration, skin aging and the development of skin cancer is widely known. As a part of this study, the effect of extracts from three varieties of Cornus mas L. ( C. mas L.) on skin cells exposed to UVA radiation was assessed. The analyses were performed on both normal and cancer skin cells. For this purpose, the potential photoprotective effects of the obtained extracts (aqueous and ethanolic) was assessed by performing two cytotoxicity tests (Alamar blue and Neutral red). Additionally, the antioxidant capacity was compared using three different assays. The 2',7'-dichlorodihydrofluorescein diacetate (H 2 DCFDA) probe was used to evaluate the intracellular level of free radicals in cells exposed to the simultaneous action of UVA radiation and dogwood extracts. Additionally, the ability to inhibit excessive pigmentation was determined by assessing the inhibition of melanin formation and tyrosinase activity. The obtained results confirmed the strong antioxidant properties of dogwood extracts and their photoprotective effect on normal skin cells. The ability to inhibit the viability of melanoma cells was also observed. Additionally, a reduction in oxidative stress in skin cells exposed to UVA radiation and a strong inhibition of melanin formation and tyrosinase activity have been demonstrated. This study shows that dogwood extract could be a valuable cosmetic raw material that can play both a photoprotective and antihyperpigmentation role in cosmetic preparations.

Skin cancer is one of the most common malignancies worldwide. Cold atmospheric pressure Plasma (CAP) is increasingly successful in skin cancer therapy, but further research is needed to understand its selective effects on cancer cells at the molecular level. In this study, A431 (squamous cell carcinoma) and HaCaT (non-malignant) cells cultured under identical conditions revealed similar ROS levels but significantly higher antioxidant levels in unstimulated A431 cells, indicating a higher metabolic turnover typical of tumour cells. HaCaT cells, in contrast, showed increased antioxidant levels upon CAP stimulation, reflecting a robust redox adaptation. Specifically, proteins involved in antioxidant pathways, including NF-κB, IκBα, Nrf2, Keap1, IKK, and pIKK, were quantified, and their translocation level upon stimulation was evaluated. CAP treatment significantly elevated Nrf2 nuclear translocation in non-malignant HaCaT cells, indicating a strong protection against oxidative stress, while selectively inducing NF-κB activation in A431 cells, potentially leading to apoptosis. The expression of pro-inflammatory genes like IL-1B , IL-6 , and CXCL8 was downregulated in A431 cells upon CAP treatment. Notably, CAP enhanced the expression of antioxidant response genes HMOX1 and GPX1 in non-malignant cells. The differential response between HaCaT and A431 cells underscores the varied antioxidative capacities, contributing to their distinct molecular responses to CAP-induced oxidative stress.