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Métodos Terapêuticos e Terapias MTCI
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1.
Biol Pharm Bull ; 43(10): 1451-1454, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32999155

RESUMO

Hair follicular keratinocyte stem cells (HFKSC) which provide a functional niche for melanocyte stem cells (MSC) are the primary target of hair graying. However, little research has been done on anti-hair graying medicines targeting HFKSC. We focused on Eriodictyon angustifolium (Ea), which reduces human hair graying when applied topically. To investigate the protective effect of dietary Ea tea (EaT) on hair pigmentation, we used an acute mouse model of hair graying that mimics X-ray-induced DNA damage associated with age-related hair graying. Our results suggest that dietary EaT maintained the niche HFKSC function against X-ray-induced DNA damage and hair graying. These results indicate that dietary EaT may prevent age-related hair graying and serve as an anti-hair graying herbal medicine.


Assuntos
Dano ao DNA/efeitos dos fármacos , Eriodictyon , Cor de Cabelo/efeitos dos fármacos , Folículo Piloso/efeitos dos fármacos , Extratos Vegetais/administração & dosagem , Chá , Animais , Antígenos CD34/análise , Antígenos CD34/metabolismo , Dano ao DNA/fisiologia , Cor de Cabelo/fisiologia , Folículo Piloso/metabolismo , Queratinócitos/efeitos dos fármacos , Queratinócitos/metabolismo , Camundongos , Camundongos Endogâmicos C57BL , Células-Tronco/efeitos dos fármacos , Células-Tronco/metabolismo
3.
J Toxicol Environ Health A ; 74(18): 1240-7, 2011.
Artigo em Inglês | MEDLINE | ID: mdl-21797775

RESUMO

Components of cherry trees have been used as traditional herbal remedies for various diseases. These components are known to possess antioxidative effects. However, the mechanisms underlying cherry tree component-mediated antioxidative effects remain largely unknown. This study focused on cherry leaves extract (CLE) and examined the mechanism underlying the effect of CLE on tert-butyl hydroperoxide (t-BOOH)-induced melanocytic cell death with DNA damage. Interestingly, CLE prevented t-BOOH-induced cell death with reduction in DNA damage, p38 kinase activation, and reactive oxygen species (ROS) production. CLE-mediated suppression of cell death with reduction of DNA damage, p38 kinase activity and ROS production was prevented by a thioredoxin (Trx) system inhibitor but not by a glutathione (GSH) system inhibitor. Finally, data showed that CLE prevented t-BOOH-induced reduction of Trx2 but not Trx1 and Trx reductases (TrxR1 and TrxR2) protein expression. Thus, our results suggest that CLE prevents t-BOOH-induced reduction in Trx2 expression, promotion of ROS production, activation of p38 kinase, and increase in DNA damage and that it protects against cell death.


Assuntos
Antioxidantes/farmacologia , Sobrevivência Celular/efeitos dos fármacos , Proteínas Mitocondriais/metabolismo , Estresse Oxidativo/efeitos dos fármacos , Extratos Vegetais/farmacologia , Folhas de Planta/química , Prunus/química , Tiorredoxinas/metabolismo , Linhagem Celular , Dano ao DNA/efeitos dos fármacos , Ativação Enzimática/efeitos dos fármacos , Glutationa/antagonistas & inibidores , Humanos , Melanócitos/efeitos dos fármacos , Melanócitos/metabolismo , Melanócitos/patologia , Proteínas Mitocondriais/antagonistas & inibidores , Oxidantes/toxicidade , Fitoterapia , Espécies Reativas de Oxigênio/metabolismo , Transdução de Sinais/efeitos dos fármacos , Tiorredoxinas/antagonistas & inibidores , Regulação para Cima/efeitos dos fármacos , Proteínas Quinases p38 Ativadas por Mitógeno/metabolismo , terc-Butil Hidroperóxido/toxicidade
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