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1.
Skin Pharmacol Physiol ; 27(2): 71-81, 2014.
Artigo em Inglês | MEDLINE | ID: mdl-24008587

RESUMO

BACKGROUND: Pentacyclic triterpenoids improve epidermal barrier function and induce collagen production. Here, their effects on cutaneous aging by means of objective instrumental measurements were elucidated. METHODS: Reconstituted human epidermis, cultivated keratinocytes and fibroblasts were incubated with Terminalia arjuna triterpenes (T. arjuna bark extract), and mRNA and protein expression of various genes was determined using microarray analysis, qRT-PCR and ELISA techniques. Clinical efficacy of T. arjuna bark extract versus vehicle control cream was elucidated in 30 patients and transepidermal water loss (TEWL), skin hydration and elasticity were measured. Another 30 female patients in their postmenopausal phase were treated with a similar regime, and skin sebum content, cutaneous blood microcirculation and skin density/echogenicity were assessed. RESULTS: Incubation with T. arjuna triterpenes increased FGF-2, TSP-1, TGF-ß and CTGF expression, and VEGF secretion in vitro. Elevated lactate dehydrogenase release upon sodium dodecyl sulphate challenge was reversed by the application of T. arjuna bark extract. T. arjuna bark extract decreased TEWL, improved skin moisturization, reduced scaliness and led to significantly improved skin elasticity. Also, increases in blood microflow and skin sebum content as well as improved skin thickness/echogenicity were noted on postmenopausal skin, resulting in visible reduction of sagging skin on the jowls as demonstrated by digital photography. CONCLUSION: T. arjuna bark extract appears as an innovative active ingredient that exerts versatile antiaging properties in vitro and in vivo.


Assuntos
Fármacos Dermatológicos/farmacologia , Triterpenos Pentacíclicos/farmacologia , Extratos Vegetais/farmacologia , Envelhecimento da Pele/efeitos dos fármacos , Pele/efeitos dos fármacos , Terminalia , Idoso , Animais , Células Cultivadas , Fármacos Dermatológicos/uso terapêutico , Elasticidade , Feminino , Fibroblastos/efeitos dos fármacos , Fibroblastos/metabolismo , Perfilação da Expressão Gênica , Humanos , Técnicas In Vitro , Queratinócitos/efeitos dos fármacos , Queratinócitos/metabolismo , Microcirculação/efeitos dos fármacos , Pessoa de Meia-Idade , Análise de Sequência com Séries de Oligonucleotídeos , Triterpenos Pentacíclicos/uso terapêutico , Casca de Planta , Extratos Vegetais/uso terapêutico , Pós-Menopausa , Fluxo Sanguíneo Regional/efeitos dos fármacos , Sebo/metabolismo , Pele/irrigação sanguínea , Pele/metabolismo , Absorção Cutânea , Suínos , Água/metabolismo
2.
Skin Pharmacol Physiol ; 25(6): 313-8, 2012.
Artigo em Inglês | MEDLINE | ID: mdl-22948093

RESUMO

INTRODUCTION: Keloids are the result of excessive scar tissue formation. Besides their poor aesthetic appearance, keloids can be associated with severe clinical symptoms such as pain, itching, and rigidity. Unfortunately, most therapeutic approaches remain clinically unsatisfactory. Recently, injections with botulinum toxin A (BTA) were proposed for the treatment of established keloids in a clinical trial. In this study, we aimed to verify the effects of intralesional BTA for the treatment of therapy-resistant keloids using objective measurements. In addition, the underlying molecular mechanisms were investigated using cultured keloid-derived fibroblasts. MATERIALS AND METHODS: Four patients received BTA (doses varying from 70 to 140 Speywood units per session) injected directly into their keloids every 2 months for up to 6 months. Differences in height and volume were evaluated clinically and measured with a 3-D optical profiling system. Keloid-derived fibroblasts were treated with different concentrations of BTA, and expression of collagen (COL)1A1, COL1A2, COL3A1, TGF-ß1, TGF-ß2, TGF-ß3, fibronectin-1, laminin-ß2, and α-SMA was determined by real-time quantitative PCR. MTT and BrdU assays were used to analyze the effects of BTA on fibroblast proliferation and metabolism. RESULTS: Intralesional administration of BTA did not result in regression of keloid tissue. No differences in expression of ECM markers, collagen synthesis, or TGF-ß could be observed after BTA treatment of keloid fibroblasts. In addition, cell proliferation and metabolism of keloid fibroblasts was not affected by BTA treatment. CONCLUSION: The suggested clinical efficiency of intralesional BTA for the therapy of existent keloids could not be confirmed in this study. Based on our data, the potential mechanisms of action of BTA on keloid-derived fibroblasts remain unclear.


Assuntos
Toxinas Botulínicas Tipo A/administração & dosagem , Queloide/tratamento farmacológico , Actinas/genética , Actinas/metabolismo , Proliferação de Células/efeitos dos fármacos , Colágeno/genética , Colágeno/metabolismo , Feminino , Fibroblastos/efeitos dos fármacos , Fibroblastos/metabolismo , Fibronectinas/genética , Fibronectinas/metabolismo , Humanos , Injeções Intralesionais , Queloide/genética , Queloide/metabolismo , Laminina/genética , Laminina/metabolismo , Masculino , Fator de Crescimento Transformador beta
3.
Dtsch Med Wochenschr ; 137(10): 491-4, 2012 Mar.
Artigo em Alemão | MEDLINE | ID: mdl-22374659

RESUMO

Psoriasin (S100A7) and koebnerisin (S100A15) were first identified in inflamed psoriatic skin. They have lately evolved by gene duplications within the Epidermal Differentiation Complex (chromosome 1q21) and form a novel S100 subfamily in human. Despite highest homology (>  90 %), psoriasin and koebnerisin are distinct in tissue distribution, regulation, and function. They act differently as antimicrobial peptides (AMP) and synergize to promote inflammation and cell migration as endogenous danger signals ("alarmines") and chemoattractants. Their different properties are compelling reasons to discriminate psoriasin and koebnerisin in epithelial homeostasis, inflammation and epithelial carcinogenesis.


Assuntos
Transformação Celular Neoplásica/metabolismo , Inflamação/metabolismo , Proteínas S100/metabolismo , Pele/metabolismo , Pele/patologia , Biomarcadores Tumorais , Diferenciação Celular/fisiologia , Transformação Celular Neoplásica/patologia , Humanos , Inflamação/patologia , Proteína A7 Ligante de Cálcio S100
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