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1.
Inflammation ; 35(5): 1723-31, 2012 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-22729280

RESUMO

Type I allergy is characterized by the release of granule-associated mediators, lipid-derived substances, cytokines, and chemokines by activated mast cells. To evaluate the anti-allergic effects of macelignan isolated from Myristica fragrans Houtt., we determined its ability to inhibit calcium (Ca(2+)) influx, degranulation, and inflammatory mediator production in RBL-2 H3 cells stimulated with A23187 and phorbol 12-myristate 13-acetate. Macelignan inhibited Ca(2+) influx and the secretion of ß-hexosaminidase, histamine, prostaglandin E(2), and leukotriene C(4); decreased mRNA levels of cyclooxygenase-2, 5-lipoxygenase, interleukin-4 (IL-4), IL-13, and tumor necrosis factor-α; and attenuated phosphorylation of Akt and the mitogen-activated protein kinases extracellular signal-regulated kinase, p38, and c-Jun N-terminal kinase. These results indicate the potential of macelignan as a type I allergy treatment.


Assuntos
Liberação de Histamina/efeitos dos fármacos , Hipersensibilidade/tratamento farmacológico , Mediadores da Inflamação/metabolismo , Lignanas/farmacologia , Mastócitos/imunologia , Mastócitos/metabolismo , Animais , Anti-Inflamatórios não Esteroides/farmacologia , Anti-Inflamatórios não Esteroides/uso terapêutico , Araquidonato 5-Lipoxigenase/genética , Calcimicina , Cálcio/metabolismo , Degranulação Celular/efeitos dos fármacos , Linhagem Celular Tumoral , Ciclo-Oxigenase 2/genética , Dinoprostona/metabolismo , MAP Quinases Reguladas por Sinal Extracelular/metabolismo , Interleucina-13/genética , Interleucina-4/genética , Proteínas Quinases JNK Ativadas por Mitógeno/metabolismo , Leucemia Basofílica Aguda/metabolismo , Leucotrieno C4/metabolismo , Lignanas/uso terapêutico , Mastócitos/efeitos dos fármacos , Myristica , Fosforilação/efeitos dos fármacos , Extratos Vegetais/farmacologia , Extratos Vegetais/uso terapêutico , Proteínas Proto-Oncogênicas c-akt/metabolismo , Ratos , Acetato de Tetradecanoilforbol , Fator de Necrose Tumoral alfa/genética , beta-N-Acetil-Hexosaminidases/metabolismo , Proteínas Quinases p38 Ativadas por Mitógeno/metabolismo
2.
Int J Vitam Nutr Res ; 80(2): 97-106, 2010 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-20803424

RESUMO

Soy isoflavones have been reported to decrease the risk of atherosclerosis in postmenopausal women. However, the effects of dietary consumption of soybean have not been explored. In this study, we evaluated the effects of consuming yellow soybeans, black soybeans (Glycine max), or sword beans (Canavalia gladiate) on lipid and oxidative stress levels in an ovariectomized rat model. Forty-seven nine-week-old female rats were ovariectomized, randomly divided into four groups, and fed one of the following diets for 10 weeks: a diet supplemented with casein (NC, n = 12), a diet supplemented with yellow soybean (YS, n = 12), a diet supplemented with black soybean (BS, n = 12), or a diet supplemented with sword bean (SB, n = 11). Plasma triglyceride (TG) levels in the BS and SB groups were significantly lower than that in the NC group. Notably, the BS group had significantly lower plasma total cholesterol (TC), and low-density lipoprotein cholesterol (LDL-C) levels than the other groups. Hepatic total lipid levels were significantly lower in the YS and SB groups, and cholesterol levels were significantly lower in the SB group than in the NC group. Superoxide dismutase (SOD) and catalase (CAT) activities were significantly higher in the groups fed beans compared to the NC group. Hepatic thiobarbituric acid reactive substances (TBARS) levels were also significantly lower in the BS and SB groups than the NC group. In conclusion, our results suggest that consumption of various types of beans may inhibit oxidative stress in postmenopausal women by increasing antioxidant activity and improving lipid profiles. Notably, intake of black soybean resulted in the greatest improvement in risk factors associated with cardiovascular disease.


Assuntos
Canavalia , Glycine max , Metabolismo dos Lipídeos , Lipídeos/sangue , Estresse Oxidativo , Análise de Variância , Animais , Biomarcadores/metabolismo , Caseínas/administração & dosagem , Catalase/metabolismo , Colesterol/sangue , Dieta/métodos , Modelos Animais de Doenças , Feminino , Fígado/metabolismo , Ovariectomia , Ratos , Ratos Sprague-Dawley , Superóxido Dismutase/metabolismo , Substâncias Reativas com Ácido Tiobarbitúrico/metabolismo , Triglicerídeos/sangue
3.
Planta Med ; 74(12): 1446-50, 2008 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-18683126

RESUMO

Exposure of the skin to ultraviolet (UV) induces photoaging associated with up-regulated matrix metalloproteinases (MMPs) activities and decreased collagen synthesis. We previously reported that panduratin A, a chalcone compound isolated from KAEMPFERIA PANDURATA Roxb ., decreased MMP-1 expression in UV-irradiated human skin fibroblasts. Here, we have investigated the effect of panduratin A on UV-induced activation of mitogen-activated protein kinases (MAPKs) signaling modules such as extracellular-regulated protein kinase (ERK), Jun-N-terminal kinase (JNK) and p38 kinase. Treatment with panduratin A in the range of 0.001 - 0.1 microM significantly inhibited UV-induced ERK, JNK and p38 activation. Moreover, inhibition of ERK, JNK and p38 by panduratin A resulted in decreased c-Fos expression and c-Jun phosphorylation induced by UV, which led to inhibition of activator protein-1 (AP-1) DNA binding activity. Panduratin A showed stronger activity than epigallocatechin 3- O-gallate (EGCG) known as a natural anti-aging agent. The results suggest that panduratin A can down-regulate UV-induced MMP-1 expression by inhibiting the MAPKs pathways and AP-1 activation. AP-1:activator protein-1 EGCG:epigallocatechin 3- O-gallate ERK:extracellular-regulated protein kinase JNK:c-Jun N-terminal kinase MAPK:mitogen-activated protein kinase MMP:matrix metalloproteinase UV:ultraviolet.


Assuntos
Chalconas/farmacologia , Ativação Enzimática/efeitos dos fármacos , Sistema de Sinalização das MAP Quinases/efeitos dos fármacos , Proteínas Quinases Ativadas por Mitógeno/metabolismo , Inibidores de Proteínas Quinases/farmacologia , Raios Ultravioleta , Linhagem Celular , Chalconas/química , Ativação Enzimática/efeitos da radiação , Fibroblastos , Humanos , Sistema de Sinalização das MAP Quinases/efeitos da radiação , Proteínas Quinases Ativadas por Mitógeno/antagonistas & inibidores , Fosforilação/efeitos dos fármacos , Fosforilação/efeitos da radiação , Pele/citologia , Pele/efeitos dos fármacos , Pele/efeitos da radiação
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