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Nrf2 and Snail-1 in the prevention of experimental liver fibrosis by caffeine

World Journal of Gastroenterology 2013年第47期19卷 9020-9033页

作者： Daniela Gordillo-Bastidas Edén Oceguera-Contreras Adriana Salazar-Montes Jaime González-Cuevas Luis Daniel Hernández-Ortega juan armendáriz-borunda nstitute of Molecular Biology in Medicine and Gene Therapy/CUCS University of GuadalajaraGuadalajaraJalisco 44100México

AIM:To determine the molecular mechanisms involved in experimental hepatic fibrosis prevention by caffeine(CFA).METHODS:Liver fibrosis was induced in Wistar rats by intraperitoneal thioacetamide or bile duct ligation and they were concomitantly treated with CFA(15 mg/kg per day).Fibrosis and inflammatory cell infiltrate were evaluated and classified by Knodell *** infiltrate was quantified by immunohistochemistry(anti-CD11b).Gene expression was analyzed by quantitative reverse transcription-polymerase chain reaction for collagenⅠ?(Col-1),connective tissue growth factor(CTGF),transforming growth factorβ1(TGF-β1),tumor necrosis factor alpha(TNF-α),interleukin-1(IL-1),IL-6,superoxide dismutase(SOD)and catalase(CAT).Activation of Nrf2 and Snail-1 was analyzed by ***-αexpression was proved by enzyme-linked immunosorbant assay,CAT activity was performed by ***:CFA treatment diminished fibrosis index in treated *** Knodell index showed both lower fibrosis and *** of profibrogenic genes CTGF,Col-1 and TGF-β1 and proinflammatory genes TNF-α,IL-6 and IL-1 was substantially diminished with CFA treatment with less CD11b positive *** lower values of transcriptional factor Snail-1 were detected in CFA treated rats compared with cirrhotic rats without treatment;in contrast Nrf2was increased in the presence of *** of SOD and CAT was greater in animals treated with CFA showing a strong correlation between mRNA expression and enzyme ***:Our results suggest that CFA inhibits the transcriptional factor Snail-1,down-regulating profibrogenic genes,and activates Nrf2 inducing antioxidant enzymes system,preventing inflammation and fibrosis.

关键词： Liver fibrosis Caffeine Thioacetamide Bile duct ligation Profibrogenic genes Proinflammatory cytokines Antioxidant enzymes

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MicroRNAs dysregulation in hepatocellular carcinoma: Insights in genomic medicine

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World Journal of Hepatology 2015年第11期7卷 1530-1540页

作者： Iván Lyra-González Laura E Flores-Fong Ignacio González-García David Medina-Preciado juan armendáriz-borunda Departamento de Biología Molecular y Genómica CUCS Universidad de Guadalajara Instituto de Biología Molecular en Medicina y Terapia Génica O.P.D. Hospital Civil de Guadalajara "Fray Antonio Alcalde" O.P.D. Hospital Civil de Guadalajara "juan I. Menchaca" Departamento de Biología Molecular y Genómica CUCS Universidad de Guadalajara

Hepatocellular carcinoma(HCC) is the leading primary liver cancer and its clinical outcome is still poor. MicroRNAs(mi RNAs) have demonstrated an interesting potential to regulate gene expression at post-transcriptional level. Current findings suggest that mi RNAs deregulation in cancer is caused by genetic and/or epigenetic, transcriptional and post-transcriptional modifications resulting in abnormal expression and hallmarks of malignant transformation: aberrant cell growth, cell death, differentiation, angiogenesis, invasion and metástasis. The important role of mi RNAs in the development and progression of HCC has increased the efforts to understand and develop mechanisms of control overt this single-stranded RNAs. Several studies have analyzed tumoral response to the regulation and control of deregulated mi RNAs with good results in vitro and in vivo, proving that targeting aberrant expression of mi RNAs is a powerful anticancer therapeutic. Identification of up and/or down regulated mi RNAs related to HCC has led to the discovery of new potential application for detection of their presence in the affected organism. Mi RNAs represent a relevant new target for diagnosis, prognosis and treatment in a wide variety of pathologic entities, including HCC. This manuscript intends to summarize current knowledge regarding mi RNAs and their role in HCC development.

关键词： Hepatocellular carcinoma MicroRNAs Regulation Therapeutic targets

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