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|Title:||Nitric oxide donors as neuroprotective agents after an ischemic stroke-related inflammatory reaction|
|Abstract:||Nitric oxide (NO) has been implicated in cirrhosis and might be implicated in renal failure end-stage cirrhosis. Aim: Our aim was to evaluate NO role in renal failure induced during decompensated cirrhosis, using the following inhibitors: aminoguanidine (AG), a specific inducible nitric oxide synthase (iNOS) inhibitor and NG-nitro-L-arginine methyl ester (L-NAME), a nonselective blocker of NOS isoforms. Methods: Endothelial (eNOS) and iNOS gene expression was analyzed by reverse transcriptase-polymerase chain reaction. Cirrhotic rats received a single intragastric dose of CCl4 to induce acute liver damage (ALD). Results: After ALD, aspartate aminotransferase highest levels were observed in rats treated with AG and ALT in rats treated with L-NAME. Inhibitors decreased creatinine serum levels to normal values and serum sodium levels re-established after the third day of ALD. L-NAME diminished (P<0.05) eNOS RNA renal expression. Renal iNOS with no inhibitor was overexpressed but was down-regulated by AG treatment. Liver eNOS RNA expression had a decreased expression before ALD in cirrhotic rats, but L-NAME treatment down-regulated eNOS after ALD. AG induced an important iNOS liver decrease. Conclusion: Both inhibitors improved renal function, although AG displayed a better effect and did not aggravate liver function. We concluded that NOS isoforms are implicated in the renal pathophysiologic events induced by ALD. " Blackwell Munksgaard 2005.",,,,,,"10.1111/j.1478-3231.2005.01018.x",,,"http://hdl.handle.net/20.500.12104/43152","http://www.scopus.com/inward/record.url?eid=2-s2.0-14544289526&partnerID=40&md5=9089b79cd5d5185998d8e6e9b00919f0",,,,,,"1",,"Liver International",,"131|
WOS",,,,,,"Cirrhosis; Decompensated cirrhosis; Nitric oxide; Nitric oxide expression; Nitric oxide synthases inhibition; Renal failure-end stage cirrhosis",,,,,,"Nitric oxide synthases inhibition results in renal failure improvement in cirrhotic rats",,"Article" "44926","123456789/35008",,"Godínez-Rubío, M., Laboratorio de Desarrollo y Regeneración Neural, Instituto de Neurobiología, Universidad de Guadalajara, Camino Ing. R. Padilla Sánchez, 2100, Las Agujas, 44600 Zapopan, JAL, Mexico; Rojas-Mayorquín, A.E., Departamento de Ciencias Ambientales, Instituto de Neurociencias, Universidad de Guadalajara, 45100 Guadalajara, JAL, Mexico, Departamento de Investigación Básica, Instituto Nacional de Geriatría (INGER), Periforico Sur No. 2767, Deleg. Magdalena-Contreras, 10200 México, DF, Mexico; Ortuño-Sahagún, D., Laboratorio de Desarrollo y Regeneración Neural, Instituto de Neurobiología, Universidad de Guadalajara, Camino Ing. R. Padilla Sánchez, 2100, Las Agujas, 44600 Zapopan, JAL, Mexico",,"Godinez-Rubi, M.
Ortuno-Sahagun, D.",,"2013",,"Cerebral ischemia initiates a cascade of detrimental events including glutamate-associated excitotoxicity, intracellular calcium accumulation, formation of Reactive oxygen species (ROS), membrane lipid degradation, and DNA damage, which lead to the disruption of cellular homeostasis and structural damage of ischemic brain tissue. Cerebral ischemia also triggers acute inflammation, which exacerbates primary brain damage. Therefore, reducing oxidative stress (OS) and downregulating the inflammatory response are options that merit consideration as potential therapeutic targets for ischemic stroke. Consequently, agents capable of modulating both elements will constitute promising therapeutic solutions because clinically effective neuroprotectants have not yet been discovered and no specific therapy for stroke is available to date. Because of their ability to modulate both oxidative stress and the inflammatory response, much attention has been focused on the role of nitric oxide donors (NOD) as neuroprotective agents in the pathophysiology of cerebral ischemia-reperfusion injury. Given their short therapeutic window, NOD appears to be appropriate for use during neurosurgical procedures involving transient arterial occlusions, or in very early treatment of acute ischemic stroke, and also possibly as complementary treatment for neurodegenerative diseases such as Parkinson or Alzheimer, where oxidative stress is an important promoter of damage. In the present paper, we focus on the role of NOD as possible neuroprotective therapeutic agents for ischemia/reperfusion treatment. " 2013 Marisol Godínez-Rubío et al.
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