Person:
Moreno González, Enrique

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First Name
Enrique
Last Name
Moreno González
Affiliation
Universidad Complutense de Madrid
Faculty / Institute
Medicina
Department
Area
Cirugía
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Now showing 1 - 7 of 7
  • Publication
    Age-related differences in hepatic ischemia/reperfusion: gene activation, liver injury, and protective effect of melatonin
    (Elsevier, 2012-12) Kireev, Roman A.; Cuesta Sancho, Sara; Ibarrola De Andrés, Carolina Natalia; Bela, Teresa; Moreno González, Enrique; Vara Ameigeiras, Elena María; Fernández-Tresguerres Hernández, Jesús Ángel
    Abstract Background Ischemia/reperfusion (I/R) causes functional and structural damage to liver cells, this being more pronounced with increasing age of the tissue. Melatonin is a pineal indole that has been shown to play an important role as a free radical scavenger and anti-inflammatory molecule. Material and methods The age-dependent responses to I/R were compared in 2-mo-old and 14-mo-old male Wistar rats. After 35 min of hepatic ischemia followed by 36 h of reperfusion, rats were sacrificed. Sham-operated control rats underwent the same protocol without real vascular occlusion. Animals were intraperitoneally injected with 10 mg/kg melatonin 24 h before the operation, at the time of surgery, and 12 and 24 h after it. The tissues were submitted to histopathologic evaluation. The levels of ALT and AST were analyzed in plasma. The expression of TNF-α, IL-1β, IL-10, MCP-1, IFN-γ, iNOS, eNOS, Bad, Bax, Bcl2, AIF, PCNA, and NFKB1 genes were detected by RT-PCR in hepatic tissue. Results I/R was associated with significant increases in the expression of pro-inflammatory and pro-apoptotic genes in liver. Older rats submitted to I/R were found to respond with increased liver damage as compared with young rats, with serum ALT and AST levels significantly higher than in young animals. Mature rats also showed more evident increases in expression of pro-inflammatory cytokines (IL-1β, MCP-1, and IFN-γ) as well as a decrease in the mRNA expression of IL-10 as compared with young animals. Pro-apoptotic genes (Bax, Bad, and AIF) were significantly enhanced in liver after I/R, without differences between young and mature animals. However, the expression of Bcl2 gene did not show any change. Melatonin treatment was able to lower the expression of pro-inflammatory cytokines and pro-apoptotic genes and to improve liver function, as indicated by normalization of plasma AST and ALT levels and by reduction of necrosis and microsteatosis areas. Conclusions Melatonin treatment was able to reduce the I/R-stimulated pro-inflammatory and pro-apoptotic genes in the rat liver. Since older animals showed a more marked increase in inflammation and in liver injury, the treatment was more effective in those subjects.
  • Publication
    Trasplante hepático como tratamiento de la polineuropatía amiloidótica familiar en pacientes mayores de 60 años
    (Elsevier, 2015-05-08) Marcacuzco Quinto, Alberto Alejandro; Manrique Municio, Alejandro; Jiménez Romero, Luis Carlos; Loinaz Segurola, Carmelo; Calvo Pulido, Jorge; Justo Alonso, Iago; García-Sesma Pérez-Fuentes, Álvaro; Abradelo De Usera, Manuel; Cambra Molero, Félix; Caso Maestro, Óscar; Moreno González, Enrique
    Background and objective: Familial amyloid polyneuropathy (FAP) is the most prevalent type of hereditary systemic amyloidosis. It is an autosomal dominant disease characterized by the deposition of an abnormal variant transthyretin. It has a worldwide distribution, with localized endemic areas in Portugal, Sweden and Japan. In Spain there is an endemic focus, located in Mallorca. Liver transplantation is the only curative option for patients with FAP. The aim of this study was to describe the clinical and demographic characteristics of patients transplanted with a diagnosis of PAF. Material and method: Six patients with PAF underwent liver transplantation between April 1986 and December 2012. Results: The mean age was 57.7+16 years, patients of Spanish origin were older than 60 years. All patients had progressive symptoms as mixed polyneuropathy. In 2 patients, combined heart-liver transplants sequentially were performed. Patient survival and graft was 80% at one, 3 and 5 years. Conclusions: The only effective treatment for etiologic PAF is liver transplantation. Early detection is the key to the treatment and control, avoiding the irreversible organ damage.
  • Publication
    The Flavonoid Quercetin Reverses Pulmonary Hypertension in Rats
    (Public Library of Science, 2014-12-02) Morales Cano, Daniel; Menendez, Carmen; Moreno González, Enrique; Moral Sanz, Javier; Barreira, Bianca; Pandolfi, Rachele; Moreno Gutiérrez, Laura; Cogolludo Torralba, Ángel Luis; Pérez Vizcaíno, Francisco; Sudhiranjan Gupta
    Quercetin is a dietary flavonoid which exerts vasodilator, antiplatelet and antiproliferative effects and reduces blood pressure, oxidative status and end-organ damage in humans and animal models of systemic hypertension. We hypothesized that oral quercetin treatment might be protective in a rat model of pulmonary arterial hypertension. Three weeks after injection of monocrotaline, quercetin (10 mg/kg/d per os) or vehicle was administered for 10 days to adult Wistar rats. Quercetin significantly reduced mortality. In surviving animals, quercetin decreased pulmonary arterial pressure, right ventricular hypertrophy and muscularization of small pulmonary arteries. Classic biomarkers of pulmonary arterial hypertension such as the downregulated expression of lung BMPR2, Kv1.5, Kv2.1, upregulated survivin, endothelial dysfunction and hyperresponsiveness to 5-HT were unaffected by quercetin. Quercetin significantly restored the decrease in Kv currents, the upregulation of 5-HT2A receptors and reduced the Akt and S6 phosphorylation. In vitro, quercetin induced pulmonary artery vasodilator effects, inhibited pulmonary artery smooth muscle cell proliferation and induced apoptosis. In conclusion, quercetin is partially protective in this rat model of PAH. It delayed mortality by lowering PAP, RVH and vascular remodeling. Quercetin exerted effective vasodilator effects in isolated PA, inhibited cell proliferation and induced apoptosis in PASMCs. These effects were associated with decreased 5-HT2A receptor expression and Akt and S6 phosphorylation and partially restored Kv currents. Therefore, quercetin could be useful in the treatment of PAH.
  • Publication
    Melatonin treatment protects liver of Zucker rats after ischemia/reperfusion by diminishing oxidative stress and apoptosis
    (Elsevier, 2012-12-03) Kireev, Roman; Bitoun, Samuel; Cuesta Sancho, Sara; Tejerina, Alejandro; Ibarrola De Andrés, Carolina Natalia; Moreno González, Enrique; Vara Ameigeiras, Elena María; Fernández-Tresguerres Hernández, Jesús Ángel
    Fatty livers occur in up to 20% of potential liver donors and increase cellular injury during the ischemia/reperfusion phase, so any intervention that could enable a better outcome of grafts for liver transplantation would be very useful. The effect of melatonin on liver ischemia/reperfusion injury in a rat model of obesity and hepatic steatosis has been investigated. Forty fa/fa Zucker rats were divided in 4 groups. 3 groups were subjected to 35 min of warm hepatic ischemia and 36 h of reperfusion. One experimental group remained untreated and 2 were given 10 mg/kg melatonin intraperitoneally or orally. Another group was sham-operated. Plasma ALT, AST and hepatic content of ATP, MDA, hydroxyalkenals, NOx metabolites, antioxidant enzyme activity, caspase-9 and DNA fragmentation were determined in the liver. The expression of iNOS, eNOS, Bcl2, Bax, Bad and AIF were determined by RT-PCR Melatonin was effective at decreasing liver injury by both ways as assessed by liver transaminases, markers of apoptosis, of oxidative stress and improved liver ATP content. Melatonin administration decreased the activities or levels of most of the parameters measured in a beneficial way, and our study identified also some of the mechanisms of protection. We conclude that administration of melatonin improved liver function, as well as markers of pro/antioxidant status and apoptosis following ischemia/reperfusion in obese rats with fatty liver. These data suggest that this substance could improve outcome in patients undergoing liver transplantation who receive a fatty liver implant and suggest the need of clinical trials with it in liver transplantation.
  • Publication
    Complement C3F allotype synthesized by liver recipient modifies transplantation outcome independently from donor hepatic C3.
    (Wiley, 2016-11-01) Valero Hervás, Diana María; Sánchez Zapardiel, Elena; Castro Panete, María José; Gallego Bustos, Fernando; Cambra Molero, Félix; Justo Alonso, Iago; Laguna Goya, Rocío; Jiménez Romero, Luis Carlos; Moreno González, Enrique; López Medrano, Francisco; San Juan Garrido, Rafael; Fernández Ruiz, Mario; Aguado García, José María; Paz Artal, Estela Natividad
    Complement component 3 (C3) presents both slow (C3S) and fast (C3F) variants, which can be locally produced and activated by immune system cells. We studied C3 recipient variants in 483 liver transplant patients by RT-PCR-HRM to determine their effect on graft outcome during the first year post-transplantation. Allograft survival was significantly decreased in C3FF recipients (C3SS 95% vs C3FS 91% vs C3FF 83%; P=.01) or C3F allele carriers (C3F absence 95% vs C3F presence 90%, P=.02). C3FF genotype or presence of C3F allele independently increased risk for allograft loss (OR: 2.38, P=.005 and OR: 2.66, P=.02, respectively). C3FF genotype was more frequent among patients whose first infection was of viral etiology (C3SS 13% vs C3FS 18% vs C3FF 32%; P=.04) and independently increased risk for post-transplant viral infections (OR: 3.60, P=.008). On the other hand, C3FF and C3F protected from rejection events (OR: 0.54, P=.03 and OR: 0.63, P=.047, respectively). Differences were not observed in hepatitis C virus recurrence or patient survival. In conclusion, we show that, independently from C3 variants produced by donor liver, C3F variant from recipient diminishes allograft survival, increases susceptibility to viral infections, and protects from rejection after transplantation. C3 genotyping of liver recipients may be useful to stratify risk.
  • Publication
    Trasplante hepático como tratamiento de la polineuropatía amiloidótica familiar en pacientes mayores de 60 años.
    (Elsevier, 2015-05-08) Marcacuzco Quinto, Alberto Alejandro; Manrique Municio, Alejandro; Jiménez Romero, Luis Carlos; Loinaz Segurola, Carmelo; Calvo Pulido, Jorge; Justo Alonso, Iago; García-Sesma Pérez-Fuentes, Álvaro; Abradelo De Usera, Manuel; Cambra Molero, Félix; Caso Maestro, Óscar; Moreno González, Enrique
    Fundamento y objetivo La polineuropatía amiloidótica familiar (PAF) constituye el tipo más prevalente de amiloidosis sistémica hereditaria. Es una enfermedad autosómica dominante que se caracteriza por el depósito de una variante anómala de la transtiretina. Tiene una distribución mundial, con zonas endémicas localizadas en Portugal, Suecia y Japón. En España hay un foco endémico, localizado en Mallorca. El trasplante hepático es la única opción curativa para los pacientes con PAF. El objetivo de este estudio fue describir las características clínicas y demográficas de los pacientes trasplantados con diagnóstico de PAF. Material y método Se evaluaron 6 pacientes trasplantados por PAF entre abril de 1986 y diciembre de 2012. Resultados La edad media fue de 57,7+16 años, los pacientes de origen español eran mayores de 60 años. Todos los pacientes presentaban síntomas progresivos en forma de polineuropatía mixta. En 2 pacientes se realizó un doble trasplante hepatocardiaco secuencial, efectuándose en primer lugar el trasplante hepático. La supervivencia del paciente y del injerto fue del 80% a los uno, 3 y 5 años. Conclusiones El único tratamiento etiológico eficaz para la PAF es el trasplante hepático. Una detección temprana es la clave para el tratamiento y el control, evitándose el daño orgánico irreversible.
  • Publication
    Different patterns of pulmonary vascular disease induced by type 1 diabetes and moderate hypoxia in rats
    (2012-03-21) Moral Sanz, Javier; Lopez Lopez, José G.; Menendez, Carmen; Moreno González, Enrique; Barreira, Bianca; Morales Cano, Daniel; Escolano, Lucia; Fernandez Segoviano, Pilar; Villamor, Eduardo; Cogolludo, Angel; Perez Vizcaino, Francisco; Moreno Gutiérrez, Laura
    Although type 1 and type 2 diabetes are strongly associated with systemic cardiovascular morbidity, the relationship with pulmonary vascular disease had been almost disregarded until recent epidemiological data revealed that diabetes might be a risk factor for pulmonary hypertension. Recent experimental studies suggest that diabetes induces changes in lung function insufficient to elevate pulmonary pressure. The aim of this study was to assess the effects of diabetes on the sensitivity to other risk factors for pulmonary hypertension. We therefore analysed the effects of the combination of diabetes with exposure to moderate hypoxia on classical markers of pulmonary hypertension. Control (saline-treated) and diabetic (70 mg kg-1 streptozotocin-treated) male Wistar-Kyoto rats were followed for 4 weeks and exposed to normoxia or moderate normobaric hypoxia (14%) for another 2 weeks. Hypoxia, but not diabetes, strongly reduced voltage-gated potassium currents, whereas diabetes, but not hypoxia, induced pulmonary artery endothelial dysfunction. Both factors independently induced pulmonary vascular remodelling and downregulated the lung bone morphogenetic protein receptor type 2. However, diabetes, but not hypoxia, induced pulmonary infiltration of macrophages, which was markedly increased when both factors were combined. Diabetes plus hypoxia induced a modest increase in diastolic and mean pulmonary artery pressure and right ventricular weight, while each of the two factors alone had no significant effect. The pattern of changes in markers of pulmonary hypertension was different for moderate hypoxia and diabetes, with no synergic effect except for macrophage recruitment, and the combination of both factors was required to induce a moderate elevation in pulmonary arterial pressure.