Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 2 de 2
Filtrar
Mais filtros

Métodos Terapêuticos e Terapias MTCI
Base de dados
Ano de publicação
Tipo de documento
País de afiliação
Intervalo de ano de publicação
1.
Food Res Int ; 178: 113938, 2024 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-38309866

RESUMO

Intestinal barrier integrity is essential for normal nutrient digestion and absorption and disease resistance. This study aims to investigate how fermentation affects the ameliorative effect of bee pollen on the intestinal barrier dysfunction stimulated by interferon-γ and tumor necrosis factor (IFN-γ/TNF-α) cytokines. The results indicated that fermentation enhances the alleviating effect of bee pollen on intestinal barrier dysfunction (including elevated trans epithelial electrical resistance and decreased paracellular permeability). In addition, fermented bee pollen (FBP) significantly decreased (p < 0.05) the secretion levels of interleukin (IL)-6, IL-8, and IL-1ß and expression of cyclooxygenase (COX)-2 protein in intestinal barrier cells. Furthermore, fermentation improved the ability of bee pollen to up-regulate the expression of tight junction proteins including zonula occludens (ZO)-1, occluding, and claudin-1. Notably, FBP showed stronger ability to inhibit the expression of nuclear factor kappa-B (NF-κB) mediated myosin light chain kinase (MLCK) and myosin light chain (MLC) signaling pathway associated with phosphorylated proteins. Overall, our results indicated that fermentation enhances the protective effect of bee pollen on the intestinal barrier, and FBP has promising potential to be used as a novel functional food to protect the intestinal barrier.


Assuntos
Quinase de Cadeia Leve de Miosina , NF-kappa B , Humanos , Animais , Abelhas , NF-kappa B/metabolismo , Quinase de Cadeia Leve de Miosina/metabolismo , Células CACO-2 , Fermentação , Mucosa Intestinal/metabolismo , Fator de Necrose Tumoral alfa/metabolismo , Transdução de Sinais , Pólen
2.
Nutrients ; 12(9)2020 Aug 19.
Artigo em Inglês | MEDLINE | ID: mdl-32825154

RESUMO

Nonalcoholic fatty liver disease (NAFLD) is a disorder characterized by the excess accumulation of fat in the hepatocytes. It is commonly associated with severe obesity and inflammation. Free fatty acids (FFAs) are the key to regulate lipid metabolism and immune response in hepatocyte cells. This study examined the effects of AEN (alcohol extract of nutmeg, the seed of Myristica fragrans Houtt.) on the inhibition of lipid synthesis and inflammation in vitro and in vivo and on high-fat diet-induced obesity in NAFLD mice. Our results showed that AEN treatment could downregulate the expression of lipid synthesis-related genes fatty acid synthase (FASN) and sterol regulatory element-binding protein 1c (SREBP-1c) and lower the lipid content of cells. AEN also inhibited FFAs-mediated inflammation-related cytokines interleukin-6 (IL-6) and tumor necrosis factor α (TNFα) expression in cells. In a mouse model, AEN reduced the bodyweight of obese mice and improved NAFLD without affecting food intake. Further analysis revealed that AEN significantly reduced inflammation level, cholesterol and lipid accumulation, blood glucose, and other liver function indexes in mice fed with a high-fat diet. In conclusion, AEN inhibited the aggravation of obesity and inflammation by downregulating lipid-gene expression in the liver to ameliorate NAFLD.


Assuntos
Ácidos Graxos não Esterificados/metabolismo , Inflamação/tratamento farmacológico , Myristica/química , Hepatopatia Gordurosa não Alcoólica/tratamento farmacológico , Hepatopatia Gordurosa não Alcoólica/metabolismo , Obesidade/tratamento farmacológico , Fitoterapia , Extratos Vegetais/farmacologia , Extratos Vegetais/uso terapêutico , Animais , Linhagem Celular , Modelos Animais de Doenças , Ácido Graxo Sintase Tipo I/genética , Ácido Graxo Sintase Tipo I/metabolismo , Expressão Gênica/efeitos dos fármacos , Humanos , Inflamação/prevenção & controle , Interleucina-6/metabolismo , Masculino , Camundongos , Hepatopatia Gordurosa não Alcoólica/prevenção & controle , Obesidade/prevenção & controle , Células RAW 264.7 , Proteína de Ligação a Elemento Regulador de Esterol 1/genética , Proteína de Ligação a Elemento Regulador de Esterol 1/metabolismo , Fator de Necrose Tumoral alfa/metabolismo
SELEÇÃO DE REFERÊNCIAS
DETALHE DA PESQUISA