Polydatin attenuates potassium oxonate-induced hyperuricemia and kidney inflammation by inhibiting NF-κB/NLRP3 inflammasome activation via the AMPK/SIRT1 pathway.
Food Funct
; 8(5): 1785-1792, 2017 May 24.
Article
em En
| MEDLINE
| ID: mdl-28428988
ABSTRACT
This study was designed to investigate the effects of polydatin (PLD) on potassium oxonate-induced hyperuricemic rats. Hyperuricemic rats were treated with potassium oxonate (250 mg kg-1) intragastrically for 7 days, and polydatin (25, 50 mg kg-1) or allopurinol (5 mg kg-1) was administered to the rats 1 h after the potassium oxonate exposure. Polydatin administration decreased the levels of uric acid and creatinine in serum and urine, leading to inhibition of pro-inflammatory cytokine production in serum and kidney. Western blot analyses illustrated that polydatin down-regulated the translocation of NF-κB p65, the degradation of IκBα, and the protein levels of inflammasome components (NLRP3, ASC, and caspase-1), which led to reduced IL-1ß secretion. Notably, polydatin treatment activated AMP kinase (AMPK) protein and increased SIRT1 expression. Taken together, polydatin might be a promising agent for gouty treatment to inhibit renal NF-κB/NLRP3 inflammasome activation via the AMPK/SIRT1 pathway.
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Estilbenos
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NF-kappa B
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Hiperuricemia
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Proteínas Quinases Ativadas por AMP
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Sirtuína 1
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Inflamassomos
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Proteína 3 que Contém Domínio de Pirina da Família NLR
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Glucosídeos
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Rim
Limite:
Animals
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Humans
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Male
Idioma:
En
Revista:
Food Funct
Ano de publicação:
2017
Tipo de documento:
Article