Luteolin Prevents UVB-Induced Skin Photoaging Damage by Modulating SIRT3/ROS/MAPK Signaling: An in vitro and in vivo Studies

The aim of this study was to investigate the role of luteolin in the mechanism of ultraviolet radiation B (UVB)-induced photoaging. An in vivo photoaging model was established using UVB irradiation of bare skin on the back of rats, and an in vitro photoaging model was established using UVB irradiation of human dermal fibroblasts (HDF). Skin damage was observed using hematoxylin-eosin (HE) and Masson staining, skin and cellular reactive oxygen species (ROS) levels were detected by DHE and DCF fluorescent probes, mitochondrial membrane potential was detected by JC-1 staining, and protein expressions were detected by immunofluorescence and Western Blot. Results from animal experiments showed that luteolin reduced UVB-induced erythema and wrinkle formation. Results from cellular assays showed that luteolin inhibited UVB-induced decrease in cell viability. In addition, in vitro and in vivo experiments showed that luteolin reduced oxidative stress levels, decreased activation of matrix metalloproteinases (MMPs) and increased collagen expression. Continued cellular experiments using 3-TYP, an inhibitor of Sirtuin 3 (SIRT3), revealed a loss of cellular protection by luteolin and a decrease in collagen, suggesting that luteolin acts by targeting and promoting SIRT3. luteolin is involved in the protection of skin cells against UVB radiation-induced ageing via the SIRT3/ROS/mitogen-activated protein kinases (MAPK) axis and it may be a promising therapeutic agent for the prevention of UVB photoaging.

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Effects of Probiotics in the Management of Infected Chronic Wounds: From Cell Culture to Human Studies

Current Clinical Pharmacology ◽

10.2174/1574884714666191111130630 ◽

2020 ◽

Vol 15 (3) ◽

pp. 193-206

Author(s):

Brognara Lorenzo ◽

Salmaso Luca ◽

Mazzotti Antonio ◽

Di M. Alberto ◽

Faldini Cesare ◽

...

Keyword(s):

Chronic Wounds ◽

Animal Experiments ◽

Multidrug Resistant ◽

Preliminary Evidence ◽

Human Studies ◽

In Vivo Studies ◽

Resistant Bacteria ◽

Keywords Probiotics

Background: Chronic wounds are commonly associated with polymicrobial biofilm infections. In the last years, the extensive use of antibiotics has generated several antibiotic-resistant variants. To overcome this issue, alternative natural treatments have been proposed, including the use of microorganisms like probiotics. The aim of this manuscript was to review current literature concerning the application of probiotics for the treatment of infected chronic wounds. Methods: Relevant articles were searched in the Medline database using PubMed and Scholar, using the keywords “probiotics” and “wound” and “injuries”, “probiotics” and “wound” and “ulcer”, “biofilm” and “probiotics” and “wound”, “biofilm” and “ulcer” and “probiotics”, “biofilm” and “ulcer” and “probiotics”, “probiotics” and “wound”. Results: The research initially included 253 articles. After removal of duplicate studies, and selection according to specific inclusion and exclusion criteria, 19 research articles were included and reviewed, accounting for 12 in vitro, 8 in vivo studies and 2 human studies (three articles dealing with animal experiments included also in vitro testing). Most of the published studies about the effects of probiotics for the treatment of infected chronic wounds reported a partial inhibition of microbial growth, biofilm formation and quorum sensing. Discussion: The application of probiotics represents an intriguing option in the treatment of infected chronic wounds with multidrug-resistant bacteria; however, current results are difficult to compare due to the heterogeneity in methodology, laboratory techniques, and applied clinical protocols. Lactobacillus plantarum currently represents the most studied strain, showing a positive application in burns compared to guideline treatments, and an additional mean in chronic wound infections. Conclusions: Although preliminary evidence supports the use of specific strains of probiotics in certain clinical settings such as infected chronic wounds, large, long-term clinical trials are still lacking, and further research is needed.

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Abstract 518: In Vitro and in vivo Disease Modeling Using Patient Derived iPSCs to Characterize the Calcification Phenotype in Arterial Calcification Due to Deficiency of CD73

Arteriosclerosis Thrombosis and Vascular Biology ◽

10.1161/atvb.36.suppl_1.518 ◽

2016 ◽

Vol 36 (suppl_1) ◽

Author(s):

Cynthia St. Hilaire ◽

Hui Jin ◽

Yuting Huang ◽

Dan Yang ◽

Alejandra Negro ◽

...

Keyword(s):

Vascular Calcification ◽

Disease Modeling ◽

Induced Pluripotent Stem Cell ◽

Dermal Fibroblasts ◽

In Vivo Studies ◽

Arterial Calcification ◽

Patient Specific ◽

And Control

Objective: The objective of this study was to develop a patient-specific induced pluripotent stem cell (iPSC)-based disease model to understand the process by which CD73-deficiency leads to vascular calcification in the disease, Arterial Calcification due to Deficiency of CD73 (ACDC). Approach & Results: ACDC is an autosomal recessive disease resulting from mutations in the gene encoding for CD73, which converts extracellular AMP to adenosine. CD73-deficiency manifests with tortuosity and vascular calcification of the medial layer of lower-extremity arteries, a pathology associated with diabetes and chronic kidney disease. We previously identified that dermal fibroblasts isolated from ACDC patients calcify in vitro, however in vivo studies of the vasculature are limited, as murine models of CD73 deficiency do not recapitulate the human disease phenotype. Thus, we created iPSCs from ACDC patients and control fibroblasts. ACDC and Control iPSCs form teratomas when injected in immune-compromised mice, however ACDC iPSC teratomas exhibit extensive calcifications. Control and ACDC iPSCs were differentiated down the mesenchymal lineage (MSC) and while there was no difference in chondrogenesis and adipogenesis, ACDC iMSCs underwent osteogenesis sooner than control iPSC, have higher activity of tissue-nonspecific alkaline phosphatase (TNAP), and lower levels of extracellular adenosine. During osteogenic simulation, TNAP activity in ACDC cells significantly increased adenosine levels, however, not to levels needed for functional compensatory stimulation of the adenosine receptors. Inhibition of TNAP with levimisole ablates this increase in adenosine. Treatment with an A2b adenosine receptor (AR) agonist drastically reduced TNAP activity in vitro, and calcification in ACDC teratomas, as did treatment with etidronate, which is currently being tested in a clinical trial on ACDC patients. Conclusions: These results illustrate a pro-osteogenic phenotype in CD73-deficient cells whereby TNAP activity attempts to compensate for CD73 deficiency, but subsequently induces calcification that can be reversed by activation of the A2bAR. The iPSC teratoma model may be used to screen other potential therapeutics for calcification disorders.

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Paraquat Poisoning by Skin Absorption: A Review

Human Toxicology ◽

10.1177/096032718800700103 ◽

1988 ◽

Vol 7 (1) ◽

pp. 15-19 ◽

Cited By ~ 40

Author(s):

J.G. Smith

Keyword(s):

Human Skin ◽

Animal Experiments ◽

Systemic Absorption ◽

In Vitro Tests ◽

Skin Damage ◽

Fatal Poisoning ◽

Head Restraint ◽

Paraquat Poisoning

All reported cases of paraquat poisoning by absorption through the skin are briefly reviewed. It is concluded that, while paraquat cannot be absorbed significantly through intact human skin, damage to the skin, either by paraquat itself or by other means, will permit greater systemic absorption and possibly poisoning. The lowest known concentration of paraquat to result in fatal poisoning through the skin is 5 g/l. Animal experiments with paraquat are also reviewed. The fact that the reported lethal dermal dose of paraquat in rats is slightly less than the oral dose is probably due to the lack of head restraint on the rats in the dermal dosing experiments. In vivo and in vitro tests on human skin at concentrations of 9 g/l and 5 g/l did not result in significant absorption of paraquat through the skin but in these experiments the skin was intact.

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Almond Consumption Increased UVB Resistance in Healthy Asian Women

Current Developments in Nutrition ◽

10.1093/cdn/nzab037_029 ◽

2021 ◽

Vol 5 (Supplement_2) ◽

pp. 319-319

Author(s):

Susanne Henning ◽

Jason Li ◽

Gail Thames ◽

Omar Bari ◽

Patrick Tran ◽

...

Keyword(s):

Skin Aging ◽

Ultraviolet B ◽

In Vivo Studies ◽

Asian Women ◽

Skin Extract ◽

Uvb Radiation ◽

Facial Skin ◽

Uvb Exposure

Abstract Objectives Almonds are a rich source of phenolic and polyphenolic compounds, which have antioxidant activity. In vitro and in vivo studies have demonstrated that topical application of almond oil and almond skin extract reduces UVB-induced photoaging. Ultraviolet-B (UVB) protection by oral almond consumption has not been previously studied in humans. It was the objective to investigate whether oral almond consumption can increase resistance to UVB radiation and reduce skin aging in healthy Asian women. Methods Thirty-nine female participants (18–45 years) with Fitzpatrick skin type II-IV were randomly assigned to consume either 1.5 oz of almonds or 1.8 oz of pretzels daily for 12 weeks. Minimal erythema dose (MED) was determined using a standardized protocol, which determined the minimal radiation inducing erythema on the inner arm 24 hours following UVB exposure. Facial skin texture was evaluated by two dermatologists using the Clinician's Erythema Assessment scale and Allergan Roughness scale. Facial melanin index, hydration, sebum, and erythema were determined using a cutometer. Results Women who consumed almonds, experienced a significant increase in MED from 415 ± 64 to 487 ± 59 (18.7 ± 19.2%, P = 0.006) from baseline to week 12 compared to women in the pretzel group from 415 ± 67 to 421 ± 67 (1.8 ± 11.1%). The exposure time to reach minimal erythema was also increased significantly in the almond group from 160 ± 23 to 187 ± 25 (17.5 ± 22.2%) compared to the pretzel group from 165 ± 27 to 166 ± 25 (1.7 ± 14%) (p=0.026). There were no differences noted between the groups consuming almonds versus pretzels in Allergan roughness, melanin, hydration, or sebum on facial skin. Conclusions Our findings suggest that daily oral almond consumption may lead to enhanced protection from UVB photodamage by increasing the MED. Protection from other UV radiation was not tested and therefore almond consumption will not replace other methods of sun protection such as application of sunscreen or wearing protective closing. Funding Sources Almond Board of California.

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In Vitro and In Vivo Photoprotective Effects of (-)-Loliode Isolated from the Brown Seaweed, Sargassum horneri

Molecules ◽

10.3390/molecules26226898 ◽

2021 ◽

Vol 26 (22) ◽

pp. 6898

Author(s):

Lei Wang ◽

Hyun-Soo Kim ◽

Jun-Geon Je ◽

Xiaoting Fu ◽

Caoxing Huang ◽

...

Keyword(s):

Brown Seaweed ◽

Human Keratinocytes ◽

Dermal Fibroblasts ◽

Sargassum Horneri ◽

Skin Damage ◽

In Vivo Models ◽

In Vivo Test ◽

Skin Cells

Skin is the largest organ of humans. Overexposure to ultraviolet (UV) is the primary environmental factor that causes skin damage. The compound, (-)-loliode, isolated from the brown seaweed Sargassum horneri, showed strong antioxidant and anti-inflammatory activities in in vitro and in vivo models. To further explore the potential of (-)-loliode in cosmetics, in the present study, we investigated the photoprotective effect of (-)-loliode in vitro in skin cells and in vivo in zebrafish. The results indicated that (-)-loliode significantly reduced intracellular reactive oxygen species (ROS) level, improved cell viability, and suppressed apoptosis of UVB-irradiated human keratinocytes. In addition, (-)-loliode remarkably attenuated oxidative damage, improved collagen synthesis, and inhibited matrix metalloproteinases expression in UVB-irradiated human dermal fibroblasts. Furthermore, the in vivo test demonstrated that (-)-loliode effectively and dose-dependently suppressed UVB-induced zebrafish damage displayed in decreasing the levels of ROS, nitric oxide, lipid peroxidation, and cell death in UVB-irradiated zebrafish. These results indicate that (-)-loliode possesses strong photoprotective activities and suggest (-)-loliode may an ideal ingredient in the pharmaceutical and cosmeceutical industries.

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Pinocembrin Ameliorates Skin Fibrosis via Inhibiting TGF-β1 Signaling Pathway

Biomolecules ◽

10.3390/biom11081240 ◽

2021 ◽

Vol 11 (8) ◽

pp. 1240

Author(s):

Xiaohe Li ◽

Yunqian Zhai ◽

Buri Xi ◽

Wei Ma ◽

Jianwei Zhang ◽

...

Keyword(s):

Therapeutic Potential ◽

Potential Effect ◽

Dermal Fibroblasts ◽

Skin Fibrosis ◽

In Vivo Studies ◽

Migration And Invasion ◽

Therapeutic Modalities ◽

Tgf Β1

Skin fibrotic diseases, such as keloids, are mainly caused by pathologic scarring of wounds during healing and characterized by benign cutaneous overgrowths of dermal fibroblasts. Current surgical and therapeutic modalities of skin fibrosis are unsatisfactory. Pinocembrin, a natural flavonoid, has been shown to possess a vast range of pharmacological activities including antimicrobial, antioxidant, anti-inflammatory, and anti-tumor activities. In this study we explored the potential effect and mechanisms of pinocembrin on skin fibrosis in vitro and in vivo. In vitro studies indicated that pinocembrin dose-dependently suppressed proliferation, migration, and invasion of keloid fibroblasts and mouse primary dermal fibroblasts. The in vivo studies showed that pinocembrin could effectively alleviate bleomycin (BLM)-induced skin fibrosis and reduce the gross weight and fibrosis-related protein expression of keloid tissues in xenograft mice. Further mechanism studies indicated that pinocembrin could suppress TGF-β1/Smad signaling and attenuate TGF-β1-induced activation of skin fibroblasts. In conclusion, our results demonstrate the therapeutic potential of pinocembrin for skin fibrosis.

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Characterization and In Vivo Studies of Nanothickness Ca- and P-Based Coatings

Key Engineering Materials ◽

10.4028/www.scientific.net/kem.361-363.649 ◽

2007 ◽

Vol 361-363 ◽

pp. 649-652

Author(s):

Paulo Guilherme Coelho ◽

Marcelo Suzuki ◽

C.A.O. Fernandes ◽

G. Cardaropoli

Keyword(s):

Ion Beam ◽

Animal Experiments ◽

Biomechanical Testing ◽

Depth Profiling ◽

Thickness Effect ◽

In Vivo Studies ◽

Tof Sims ◽

Bioceramic Coatings

Objective: This series of laboratorial and in-vivo studies describe the characterization, evolution, and in-vivo performance of various Ca- and P-based nanothicknesses and microstructures ion beam assisted depositions (IBAD) onto Ti-6Al-4V implants. Materials and Methods: Characterization- The 4 mm in diameter and 10 mm in length implant rods (Ti-6Al-4V) with IBAD I, IBAD II, and control (alumina-blasted/acid-etched, AB/AE) surfaces were provided by an implant manufacturer. The in-vitro characterization comprised the following techniques: (1) SEM/EDS, (2) XPS/Depth Profiling (3) Thin-film XRD (4) AFM + ToF-SIMS for coating thickness determination (5) AFM- Ra determination. In-vivo- Three animal experiments were carried out for evaluation of the nanothickness bioceramic coatings. All experiments comprised a proximal tibia model with 4-6 implants placed along the bones. Times in-vivo ranged from 2-5 weeks. Static (bioactivity, bone to implant contact) and dynamic (mineral apposition rates- MAR) histomorphometric measurements were recorded. Biomechanical testing was performed by pullout and torque to interfacial failure testing. Results: Combination of the characterization techniques showed that all bioceramic coatings were Ca- and P-based bioceramics of amorphous microstructure. AFM +ToF-SIMS showed that IBAD II coatings were thicker (300-500 nm) compared to IBAD I coatings (30-50 nm). Surface roughness did not change significantly for the IBAD implant groups compared to control. The in-vivo results showed higher degrees of osseoactivity, torque to failure, and MAR for the coated implants at different times in-vivo. IBAD II had higher biomechanical fixation at early implantation times compared to other groups. Conclusions: The results obtained in the in-vitro part this study support that both IBAD I and IBAD II coatings are Ca- and P- based amorphous bioceramics in the nanothickness range with theoretical high dissolution rates. The increased osseoactivity observed for IBAD coated and the high MAR values observed for IBAD coated compared to AB/AE implants support the effect of the bioceramic coating presence in the overall bone healing. A thickness effect was reveled through biomechanical testing where IBAD II (300-500nm thickness) presented higher performance.

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The Use of Antithrombotic Therapies in Reducing Synthetic Small-Diameter Vascular Graft Thrombosis

Vascular and Endovascular Surgery ◽

10.1177/1538574411433299 ◽

2012 ◽

Vol 46 (3) ◽

pp. 212-222 ◽

Cited By ~ 24

Author(s):

Mark Tatterton ◽

Stacy-Paul Wilshaw ◽

Eileen Ingham ◽

Shervanthi Homer-Vanniasinkam

Keyword(s):

Vascular Graft ◽

Animal Experiments ◽

Small Diameter ◽

In Vitro Models ◽

In Vivo Studies ◽

Synthetic Graft ◽

Graft Thrombosis ◽

Medline Search

Background. Thrombosis of synthetic small-diameter bypass grafts remains a major problem. The aim of this article is to review the antithrombotic strategies that have been used in an attempt to reduce graft thrombogenicity. Methods. A PubMed/MEDLINE search was performed using the search terms “vascular graft thrombosis,” “small-diameter graft thrombosis,” “synthetic graft thrombosis” combined with “antithrombotic,” “antiplatelet,” “anticoagulant,” “Dacron,” “PTFE,” and “polyurethane.” Results. The majority of studies on antithrombotic therapies have used either in vitro models or in vivo animal experiments. Many of the therapies used in these settings do show antithrombotic efficacy against synthetic graft materials. There is however, a distinct lack of human in vivo studies to further delineate the performance and limitations of therapies displaying good antithrombotic characteristics. Conclusion. Very few antithrombotic therapies have translated into clinical use. More human in vivo studies are required to assess the efficacy and safety of such therapies.

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Protective Effect of Fat Extract on UVB-Induced Photoaging In Vitro and In Vivo

Oxidative Medicine and Cellular Longevity ◽

10.1155/2019/6146942 ◽

2019 ◽

Vol 2019 ◽

pp. 1-11 ◽

Cited By ~ 5

Author(s):

Mingwu Deng ◽

Yuda Xu ◽

Ziyou Yu ◽

Xiangsheng Wang ◽

Yizuo Cai ◽

...

Keyword(s):

Cell Cycle ◽

Cell Proliferation ◽

Nude Mice ◽

Capillary Density ◽

Dermal Fibroblasts ◽

Apoptotic Cells ◽

Uvb Irradiation ◽

Dermal Thickness

Background. Nanofat can protect against ultraviolet B- (UVB-) induced damage in nude mice. Fat extract (FE) is a cell-free fraction isolated from nanofat that is enriched with a variety of growth factors. Objective. To determine whether FE can protect against UVB-induced photoaging in cultured dermal fibroblasts and in nude mice. Method. For the in vitro study, human dermal skin fibroblasts were pretreated with FE 24 h prior to UVB irradiation. Generation of reactive oxygen species (ROS) was analyzed immediately following irradiation, while cell cycle analysis was performed 24 h after UVB irradiation. Senescence-associated β-galactosidase (SA-β-gal) expression, cell proliferation, and expression of glutathione peroxidase 1 (GPX-1), catalase, superoxide dismutase-1 (SOD-1), SOD-2, and collagen type 1 (COL-1) were investigated 72 h after UVB irradiation. For the in vivo study, the dorsal skin of nude mice was irradiated with UVB and mice were then treated with FE for 8 weeks. The thickness of the dermis, capillary density, and apoptotic cells in skin tissue sections were investigated after treatment. The expression of GPX-1, catalase, SOD-2, SOD-1, and COL-1 in the tissue was also measured. Result. FE significantly increased cell proliferation and protected cells against UVB-induced cell death and cell cycle arrest. FE reduced ROS and the number of aged cells induced by UVB irradiation. FE promoted the expression of COL-1 and GPX-1 in cultured dermal fibroblasts. FE treatment of UVB-irradiated skin increased dermal thickness and capillary density, decreased the number of apoptotic cells, and promoted the expression of COL-1 and GPX-1. Conclusion. FE protects human dermal fibroblasts and the skin of nude mice from UVB-induced photoaging through its antioxidant, antiapoptotic, and proangiogenic activities.

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