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1.
Environ Toxicol ; 35(4): 518-527, 2020 Apr.
Artículo en Inglés | MEDLINE | ID: mdl-31804025

RESUMEN

Nonalcoholic steatohepatitis (NASH) is considered growing risk factor for hepatocellular carcinoma development in high-income countries. Diet- and chemically induced rodent models have been applied for the translational study of NASH-associated hepatocarcinogenesis due to their morphological and molecular similarities to the corresponding human disease. Arctium lappa L. (burdock) root tea has been extensively consumed in Traditional Chinese Medicine due to its potential therapeutic properties. Indeed, the bioactive compounds of A. lappa root, as the polyphenols, have already showed antioxidant and anti-inflammatory properties in different in vivo and in vitro bioassays. In this study, we investigated whether burdock root ethanolic extract (BRE) administration attenuates NASH-associated hepatocarcinogenesis. Eight-week-old male Wistar rats received choline-deficient high-fat diet for 8 weeks and multiple thioacetamide doses for 4 weeks in order to induce NASH and preneoplastic glutathione-S-transferase pi (GST-P)+ preneoplastic foci. Subsequently, rats were treated with BRE (100 or 200 mg/kg body weight) or vehicle by oral gavage for 2 weeks. BRE displayed high levels of chlorogenic and caffeic acids and BRE administration reduced total fatty acid and lipid hydroperoxide levels, while increasing the activities of antioxidant superoxide dismutase and catalase enzymes in the liver. Furthermore, burdock intervention diminished the size of GST-P+ remodeling preneoplastic lesions (PNLs) and displayed a trend on reducing hepatocyte proliferation (Ki-67) inside them. These findings suggest that short-term exposure to BRE alleviated remodeling PNL development in NASH-associated hepatocarcinogenesis.


Asunto(s)
Antiinflamatorios/uso terapéutico , Antioxidantes/uso terapéutico , Arctium/química , Neoplasias Hepáticas/prevención & control , Enfermedad del Hígado Graso no Alcohólico/tratamiento farmacológico , Extractos Vegetales/uso terapéutico , Lesiones Precancerosas/prevención & control , Animales , Antiinflamatorios/aislamiento & purificación , Antioxidantes/aislamiento & purificación , Antioxidantes/metabolismo , Ácidos Cafeicos , Dieta Alta en Grasa/efectos adversos , Humanos , Neoplasias Hepáticas/patología , Masculino , Medicina Tradicional China , Enfermedad del Hígado Graso no Alcohólico/patología , Extractos Vegetales/aislamiento & purificación , Raíces de Plantas/química , Lesiones Precancerosas/patología , Ratas , Ratas Wistar , Tioacetamida/toxicidad
2.
Toxicol Mech Methods ; 26(5): 362-370, 2016 Jun.
Artículo en Inglés | MEDLINE | ID: mdl-27268753

RESUMEN

OBJECTIVE: Liver fibrosis results from the perpetuation of the normal wound healing response to several types of injury. Despite the wealth of knowledge regarding the involvement of intracellular and extracellular signaling pathways in liver fibrogenesis, information about the role of intercellular communication mediated by gap junctions is scarce. METHODS: In this study, liver fibrosis was chemically induced by carbon tetrachloride in mice lacking connexin32, the major liver gap junction constituent. The manifestation of liver fibrosis was evaluated based on a series of read-outs, including collagen morphometric and mRNA analysis, oxidative stress, apoptotic, proliferative and inflammatory markers. RESULTS: More pronounced liver damage and enhanced collagen deposition were observed in connexin32 knockout mice compared to wild-type animals in experimentally triggered induced liver fibrosis. No differences between both groups were noticed in apoptotic signaling nor in inflammation markers. However, connexin32 deficient mice displayed decreased catalase activity and increased malondialdehyde levels. CONCLUSION: These findings could suggest that connexin32-based signaling mediates tissue resistance against liver damage by the modulation of the antioxidant capacity. In turn, this could point to a role for connexin32 signaling as a therapeutic target in the treatment of liver fibrosis.


Asunto(s)
Tetracloruro de Carbono/toxicidad , Enfermedad Hepática Inducida por Sustancias y Drogas/metabolismo , Conexinas/deficiencia , Cirrosis Hepática Experimental/metabolismo , Hígado/efectos de los fármacos , Animales , Antioxidantes/metabolismo , Enfermedad Hepática Inducida por Sustancias y Drogas/etiología , Enfermedad Hepática Inducida por Sustancias y Drogas/patología , Colágeno/metabolismo , Conexinas/genética , Citocinas/inmunología , Ensayo de Inmunoadsorción Enzimática , Femenino , Hígado/inmunología , Hígado/metabolismo , Hígado/patología , Cirrosis Hepática Experimental/etiología , Cirrosis Hepática Experimental/patología , Pruebas de Función Hepática , Ratones Noqueados , Reacción en Cadena en Tiempo Real de la Polimerasa , Proteína beta1 de Unión Comunicante
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