DBE-Artículos
URI permanente para esta colecciónhttps://hdl.handle.net/10953/111
Examinar
Examinando DBE-Artículos por Materia "Apoptosis"
Mostrando 1 - 2 de 2
- Resultados por página
- Opciones de ordenación
Ítem Constitutive nitric oxide synthases are responsible for the nitric oxide production in the ischemic aged cerebral cortex(Elsevier BV, 2005) Martínez-Lara, Esther; Cañuelo, Ana; Siles, Eva; Hernández-Cobo, Raquel; del-Moral, María Luisa; Blanco-Ruiz, Santos; Pedrosa-Raya, Juan ángel; Rodrigo, José; Peinado-Herreros, María ÁngelesAged brain shows reduced biological plasticity to meet emergency conditions such as ischemia, a process in which nitric oxide (NO) and apoptosis have been shown to play important roles. Using a model of transient global ischemia, we have analyzed the NO system and the p53, bax and bcl-2 response in the cerebral cortex of aged rats. Although immediately after ischemia the NO level is maintained, the reperfusion period increases NO concentrations together with the following: (i) greater bulk-protein nitration mainly due to a 50-kDa immunoreactive band; (ii) an increase in p53 protein; and (iii) an up-regulation of Bax together with a down-regulation of Bcl-2. These results match up with induced endothelial nitric oxide synthase expression immediately after ischemia and in neuronal nitric oxide synthase with the reperfusion. However, inducible nitric oxide synthase was not altered with ischemia/reperfusion. Altogether, these data suggest that NO production in cerebral cortex of aged ischemic animals is due to the constitutive NO synthase isoforms. This response is accompanied by the increased expression of pro-apoptotic proteins.Ítem Is endothelial-nitric-oxide-synthase-derived nitric oxide involved in cardiac hypoxia/reoxygenation-related damage?(Indian Academy of Sciences, 2011) Rus-Martínez, Alma; Peinado-Herreros, María Ángeles; Blanco-Ruiz, Santos; del-Moral, María LuisaNitric oxide (NO) has been reported to act both as a destructive and a protective agent in the pathogenesis of the injuries that occur during hypoxia/reoxygenation (H/R). It has been suggested that this dual role of NO depends directly on the isoform of NO synthase (NOS) involved. In this work, we investigate the role that NO derived from endothelial NOS (eNOS) plays in cardiac H/R-induced injury. Wistar rats were submitted to H/R (hypoxia for 30 min; reoxygenation of 0 h, 12 h and 5 days), with or without prior treatment using the selective eNOS inhibitor L-NIO (20 mg/kg). Lipid peroxidation, apoptosis and protein nitration, as well as NO production (NOx), were analysed. The results showed that L-NIO administration lowered NOx levels in all the experimental groups. However, no change was found in the lipid peroxidation level, the percentage of apoptotic cells or nitrated protein expression, implying that eNOS-derived NO may not be involved in the injuries occurring during H/R in the heart. We conclude that LNIO would not be useful in alleviating the adverse effects of cardiac H/R.