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Biomed Pharmacother ; 117: 109110, 2019 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-31252263

RESUMO

Resveratrol has been suggested to mediate liver fibrosis. The switch from classically M(LPS) to alternatively activated M(IL-4) macrophages shows to protect organs from fibrosis. However, the mechanisms remain unclear. The study aimed to investigate whether resveratrol inhibited liver fibrosis by delivering IL-10 to promote the macrophage polarization in vitro and in vivo. We observed that resveratrol improved CCL4-induced liver fibrosis, upregulated Kupffer cells, increased the expression of IL-10 and M(IL-4) marks including Mrc1, Mrc2, CD163 and Arg1, whereas it slightly suppressed the level of M(LPS) including iNOS, TNF-α and MCP1. In vitro, resveratrol promoted the M(LPS) switch to M(IL-4) macrophage and elevated the expression of CD206 and iNOS as well. Meanwhile, IL-10 increased in both M(IL-4) and M(LPS). We concluded that resveratrol relieved liver fibrosis by producing more IL-10 to promote the polarization of M(LPS) to M(IL-4)-like macrophages.


Assuntos
Interleucina-4/farmacologia , Lipopolissacarídeos/farmacologia , Cirrose Hepática/genética , Macrófagos/metabolismo , Resveratrol/farmacologia , Regulação para Cima/efeitos dos fármacos , Animais , Tetracloreto de Carbono , Polaridade Celular/efeitos dos fármacos , Inflamação/patologia , Interleucina-10/metabolismo , Macrófagos do Fígado/efeitos dos fármacos , Macrófagos do Fígado/metabolismo , Cirrose Hepática/induzido quimicamente , Macrófagos/efeitos dos fármacos , Masculino , Camundongos , Camundongos Endogâmicos BALB C , Fenótipo , Células RAW 264.7
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