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Mol Med Rep ; 18(2): 1682-1691, 2018 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-29845244

RESUMO

The aim of the present study was to explore the effect of Bushen recipe and its disassembled prescriptions on liver injury and chronic hepatitis B. Liver injury was induced in normal and hepatitis B virus (HBV)­transgenic mice through injection of Concanavalin A, followed by treatment with Bushen recipe and its disassembled prescriptions including the Bushen­yang, the Bushen­yin and the QingHua groups as well as the GanYanLing group (positive control). Subsequently, their liver function indexes were investigated by a microplate method and liver sections were blindly evaluated using an optical microscope by a pathologist. Subsequently, the activation state of Toll­like receptor (TLR)3/9 signaling pathway in liver tissues was analyzed by western blotting. Additionally, the inflammatory factors produced following liver injury in peripheral blood were detected via ELISA. Following intervention with the Bushen recipe and its disassembled prescriptions, the liver function indexe alanine aminotransferase had declined, whereas cholinesterase increased. The pathological alterations of liver tissue in HBV transgenic mice were reversed by Bushen recipe and its disassembled prescriptions. In addition, the TLR3/9 signaling pathway in liver tissues of HBV transgenic mice was inhibited and inflammatory factors such as interleukin (IL)­6, IL­1, tumor necrosis factor­α and interferon­Î³ were reduced significantly. In conclusion, the present study demonstrated that Bushen recipe and its disassembled prescriptions repaired liver injury induced by Concanavalin A through inhibition of TLR3/9 signaling pathway.


Assuntos
Anti-Inflamatórios/farmacologia , Doença Hepática Induzida por Substâncias e Drogas/tratamento farmacológico , Medicamentos de Ervas Chinesas/farmacologia , Genoma , Receptor 3 Toll-Like/genética , Receptor Toll-Like 9/genética , Animais , Doença Hepática Induzida por Substâncias e Drogas/genética , Doença Hepática Induzida por Substâncias e Drogas/imunologia , Doença Hepática Induzida por Substâncias e Drogas/patologia , Concanavalina A , Regulação da Expressão Gênica , Vírus da Hepatite B/genética , Interferon gama/antagonistas & inibidores , Interferon gama/genética , Interferon gama/imunologia , Interleucina-1/antagonistas & inibidores , Interleucina-1/genética , Interleucina-1/imunologia , Interleucina-6/antagonistas & inibidores , Interleucina-6/genética , Interleucina-6/imunologia , Masculino , Camundongos , Camundongos Transgênicos , Transdução de Sinais , Receptor 3 Toll-Like/antagonistas & inibidores , Receptor 3 Toll-Like/imunologia , Receptor Toll-Like 9/antagonistas & inibidores , Receptor Toll-Like 9/imunologia , Fator de Necrose Tumoral alfa/antagonistas & inibidores , Fator de Necrose Tumoral alfa/genética , Fator de Necrose Tumoral alfa/imunologia , Integração Viral
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