Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 3 de 3
Filtrar
Mais filtros











Base de dados
Intervalo de ano de publicação
1.
Int J Biol Macromol ; 270(Pt 1): 132093, 2024 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-38710247

RESUMO

Long-term and excessive alcohol consumption can lead to the development of alcoholic liver disease (ALD), characterized by oxidative damage, intestinal barrier injury, and disruption of intestinal microbiota. In this study, we extracted fucoidan (Aj-FUC) from Apostichopus japonicus using enzymatic methods and characterized its structure. The ALD model was established in male Balb/c mice using 56° Baijiu, with silymarin as a positive control. Mice were orally administered 100 mg/kg·bw and 300 mg/kg·bw of Aj-FUC for 28 days to evaluate its effects on liver injury in ALD mice and explore its potential role in modulating the gut-liver axis. The results showed significant improvements in histopathological changes and liver disease in the Aj-FUC group. Aj-FUC treatment significantly increased the levels of glutathione (GSH) and glutathione peroxidase (GSH-Px) while weakly reduced the elevation of malondialdehyde (MDA) induced by ALD. It also regulated the Nrf2/HO-1 signaling pathway, collectively alleviating hepatic oxidative stress. Aj-FUC intervention upregulated the expression of ZO-1 and Occludin, thus contributing to repair the intestinal barrier. Additionally, Aj-FUC increased the content of short-chain fatty acids (SCFAs) and regulated the imbalance in gut microbiota. These results suggested that Aj-FUC alleviates ALD by modulating the gut-liver axis homeostasis. It may prove to be a useful dietary supplement in the treatment of alcoholic liver damage.


Assuntos
Homeostase , Hepatopatias Alcoólicas , Fígado , Estresse Oxidativo , Polissacarídeos , Stichopus , Animais , Hepatopatias Alcoólicas/tratamento farmacológico , Hepatopatias Alcoólicas/metabolismo , Hepatopatias Alcoólicas/patologia , Polissacarídeos/farmacologia , Polissacarídeos/química , Camundongos , Masculino , Fígado/efeitos dos fármacos , Fígado/metabolismo , Fígado/patologia , Homeostase/efeitos dos fármacos , Estresse Oxidativo/efeitos dos fármacos , Stichopus/química , Camundongos Endogâmicos BALB C , Malondialdeído/metabolismo , Microbioma Gastrointestinal/efeitos dos fármacos , Glutationa/metabolismo , Fator 2 Relacionado a NF-E2/metabolismo , Transdução de Sinais/efeitos dos fármacos , Modelos Animais de Doenças , Glutationa Peroxidase/metabolismo
2.
Mol Nutr Food Res ; 67(16): e2300076, 2023 08.
Artigo em Inglês | MEDLINE | ID: mdl-37177891

RESUMO

SCOPE: Cachexia, which is often marked by skeletal muscular atrophy, is one of the leading causes of death in cancer patients. Astaxanthin, a carotenoid obtained from marine organisms that can aid in the prevention and treatment of a variety of disorders. In this study, to assess whether astaxanthin ameliorates weight loss and skeletal muscle atrophy in sorafenib-treated hepatocellular carcinoma mice is aimed. METHODS AND RESULTS: H22 mice are treated with 30 mg kg-1  day-1 of sorafenib and 60 mg kg-1  day-1 of astaxanthin by gavage lasted for 18 days. Sorafenib does not delay skeletal muscle atrophy and weight loss, although it does not reduce tumor burden. Astaxanthin dramatically delays weight loss and skeletal muscle atrophy in sorafenib-treating mice, without affecting the food intake. Astaxanthin inhibits the tumor glycolysis, slows down gluconeogenesis, and improves insulin resistance in tumor-bearing mice. Astaxanthin increases glucose competition in skeletal muscle by targeting the PI3K/Akt/GLUT4 signaling pathway, and enhances glucose utilization efficiency in skeletal muscle, thereby slowing skeletal muscle atrophy. CONCLUSION: The findings show the significant potential of astaxanthin as nutritional supplements for cancer patients, as well as the notion that nutritional interventions should be implemented at the initiation of cancer treatment, as instead of waiting until cachexia sets in.


Assuntos
Caquexia , Glucose , Camundongos , Animais , Caquexia/tratamento farmacológico , Caquexia/etiologia , Sorafenibe/farmacologia , Sorafenibe/metabolismo , Glucose/metabolismo , Fosfatidilinositol 3-Quinases/metabolismo , Atrofia Muscular/tratamento farmacológico , Atrofia Muscular/etiologia , Atrofia Muscular/metabolismo , Músculo Esquelético/metabolismo , Redução de Peso , Suplementos Nutricionais
3.
Carbohydr Polym ; 280: 119033, 2022 Mar 15.
Artigo em Inglês | MEDLINE | ID: mdl-35027135

RESUMO

Bacteria-induced wound infections and multifunctional hydrogels have received widespread attention in wound repair. In this study, self-assembling peptides (SAPs) were grafted on O-carboxymethyl chitosan (O-CMCS), and compact spatial structure and good drug sustained-release effect on mel-d1, a new AMP designed based on melittin with the same antimicrobial activity but lower cytotoxicity and ciprofloxacin (CIP) were obtained. In vivo test showed that the O-CMCS/SAP hydrogel loaded with CIP and mel-d1 accelerated the wound closure speed caused by infection of Escherichia coli and skin tissue regeneration. Both of the enhanced interaction between O-CMCS/SAP and CIP/Mel-d1 because of the hydrophobic interaction and π-π stacking, and the potential tissue healing ability of SAP played important roles. This study provided a rational design method of O-CMCS by grafting SAPs to give a wider range of biological functions.


Assuntos
Antibacterianos/farmacologia , Bandagens , Quitosana/análogos & derivados , Ciprofloxacina/farmacologia , Infecções por Escherichia coli/terapia , Meliteno/análogos & derivados , Cicatrização , Animais , Membrana Celular/efeitos dos fármacos , Preparações de Ação Retardada , Desenho de Fármacos , Escherichia coli/efeitos dos fármacos , Hidrogéis , Interações Hidrofóbicas e Hidrofílicas , Masculino , Meliteno/química , Meliteno/farmacologia , Camundongos , Camundongos Endogâmicos BALB C , Células NIH 3T3 , Peptídeos/farmacologia , Reologia
SELEÇÃO DE REFERÊNCIAS
DETALHE DA PESQUISA