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|Title:||Nrf2 and Snail-1 in the prevention of experimental liver fibrosis by caffeine|
Pacheco Moises, F.P.
Alatorre Jimenez, M.A.
Celis De La Rosa, A.
|Abstract:||Mitochondrial dysfunction has been thought to contribute to Alzheimer disease (AD) pathogenesis through the accumulation of mitochondrial DNA mutations and net production of reactive oxygen species (ROS). Mitochondrial cytochrome c-oxidase plays a key role in the regulation of aerobic production of energy and is composed of 13 subunits. The 3 largest subunits (I, II, and III) forming the catalytic core are encoded by mitochondrial DNA. The aim of this work was to look for mutations in mitochondrial cytochrome c-oxidase gene II (MTCO II) in blood samples from probable AD Mexican patients. MTCO II gene was sequenced in 33 patients with diagnosis of probable AD. Four patients (12%) harbored the A8027G polymorphism and three of them were early onset (EO) AD cases with familial history of the disease. In addition, other four patients with EOAD had only one of the following point mutations: A8003C, T8082C, C8201T, or G7603A. Neither of the point mutations found in this work has been described previously for AD patients, and the A8027G polymorphism has been described previously; however, it hasn't been related to AD. We will need further investigation to demonstrate the role of the point mutations of mitochondrial DNA in the pathogenesis of AD. " 2014 Verúnica Loera-Castañeda et al.",,,,,,"10.1155/2014/794530",,,"http://hdl.handle.net/20.500.12104/43246","http://www.scopus.com/inward/record.url?eid=2-s2.0-84896117487&partnerID=40&md5=bc848dd0aafd43682b0d8e3b1c47da9b|
http://ovidsp.ovid.com/ovidweb.cgi?T=JS&CSC=Y&NEWS=N&PAGE=fulltext&D=prem&AN=24701363",,,,,,,,"International Journal of Alzheimer's Disease",,"794530",,"2014",,"Scopus
MEDLINE",,,,,,,,,,,,"Novel point mutations and A8027G polymorphism in mitochondrial-DNA-encoded cytochrome c Oxidase II gene in mexican patients with probable alzheimer disease",,"Article" "45026","123456789/35008",,"Lugo-Baruqui, A., Instituto de Biología Molecular en Medicina y Terapia Gúnica, Departamento de Biología Molecular y Genómica, CUCS, Universidad de Guadalajara, Mexico; Bautista López, C.A., OPD Hospital Civil de Guadalajara, Mexico; Armendáriz-Borunda, J., Instituto de Biología Molecular en Medicina y Terapia Gúnica, Departamento de Biología Molecular y Genómica, CUCS, Universidad de Guadalajara, Mexico, OPD Hospital Civil de Guadalajara, Mexico",,"Lugo-Baruqui, A.
Bautista Lopez, C.A.
Armendariz-Borunda, J.",,"2009",,"Hepatitis C virus (HCV) infection represents a global health problem due to its evolution to hepatic cirrhosis and hepatocellular carcinoma. The viral pathogenesis and infectious processes are not yet fully understood. The development of natural viral resistance towards the host immune system represents a major challenge for the design of alternative therapeutic interventions and development of viral vaccines. The molecular mechanisms of hepatic fibrosis are well described. New alternatives for the treatment of patients with HCV infection and hepatic cirrhosis are under intensive research. New drugs such as viral protease inhibitors and assembly inhibitors, as well as immune modulators have been studied in clinical trials. Additional alternatives include antifibrotic drugs, which reverse the hepatic cellular damage caused by HCV infection. This review makes reference to viral infective mechanisms, molecular pathways of liver fibrosis and overviews conventional and new treatments for HCV infection and liver fibrosis.",,,,,,,,,"http://hdl.handle.net/20.500.12104/43247","http://www.scopus.com/inward/record.url?eid=2-s2.0-67650090021&partnerID=40&md5=082097c7188b331b8f7b39ec74000ee5",,,,,,"2",,"Revista Medica de Chile",,"280
WOS",,,,,,"Chronic; Cirrhosis; Fibrosis; Hepacivirus; Hepatitis C",,,,,,"Novel treatments for hepatitis C viral infection and the hepatic fibrosis [Nuevos tratamientos para la infección por virus de hepatitis C y el proceso de fibrosis hepética]",,"Review" "45027","123456789/35008",,"Gordillo-Bastidas, D., Institute of Molecular Biology in Medicine and Gene Therapy/CUCS, University of Guadalajara, Guadala jara, Jalisco 44100, Mexico; Oceguera-Contreras, E., Institute of Molecular Biology in Medicine and Gene Therapy/CUCS, University of Guadalajara, Guadala jara, Jalisco 44100, Mexico; Salazar-Montes, A., Institute of Molecular Biology in Medicine and Gene Therapy/CUCS, University of Guadalajara, Guadala jara, Jalisco 44100, Mexico; González-Cuevas, J., Institute of Molecular Biology in Medicine and Gene Therapy/CUCS, University of Guadalajara, Guadala jara, Jalisco 44100, Mexico; Hernández-Ortega, L.D., Institute of Molecular Biology in Medicine and Gene Therapy/CUCS, University of Guadalajara, Guadala jara, Jalisco 44100, Mexico; Armendáriz-Borunda, J., Institute of Molecular Biology in Medicine and Gene Therapy/CUCS, University of Guadalajara, Guadala jara, Jalisco 44100, Mexico",,"Gordillo-Bastidas, D.
Armendariz-Borunda, J.",,"2013",,"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 index. Inflammatory infiltrate was quantified by immunohistochemistry (anti-CD11b). Gene expression was analyzed by quantitative reverse transcription-polymerase chain reaction for collagen I (Col-1), connective tissue growth factor (CTGF), transforming growth factor ?1 (TGF-?1), tumor necrosis factor alpha (TNF-?), interleukin-1 (IL-1), IL-6, superoxide dismutase (SOD) and catalase (CAT). Activation of Nrf2 and Snail-1 was analyzed by Western-blot. TNF-? expression was proved by enzyme-linked immunosorbant assay, CAT activity was performed by zymography. RESULTS: CFA treatment diminished fibrosis index in treated animals. The Knodell index showed both lower fibrosis and necroinflammation. Expression of profibro-genic genes CTGF, Col-1 and TGF-?1 and proinflam-matory genes TNF-?, I L- 6 and IL- 1 was substantially diminished with CFA treatment with less CD11b positive areas. Significantly lower values of transcriptional factor Snail-1 were detected in CFA treated rats compared with cirrhotic rats without treatment; in contrast Nrf2 was increased in the presence of CFA. Expression of SOD and CAT was greater in animals treated with CFA showing a strong correlation between mRNA expression and enzyme activity. CONCLUSION: Our results suggest that CFA inhibits the transcriptional factor Snail-1, down-regulating profi-brogenic genes, and activates Nrf2 inducing antioxidant enzymes system, preventing inflammation and fibrosis. " 2013 Baishideng Publishing Group Co., Limited. All rights reserved.
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