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Gonçalves Renata C. Carvalho Celso Carneiro Michels Monique Abatti Mariane R. Manfredini Andressa Silva Milena C. Dominguini Diogo Steckert Amanda Mina Francielle Streck Emílio Budni Josiane Dal-Pizzol Felipe 《Neurochemical research》2022,47(3):613-621
Neurochemical Research - Critical illness encompasses a wide spectrum of life-threatening clinical conditions requiring intensive care. Our objective was to evaluate cognitive, inflammatory and... 相似文献
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Mauricio?P.?Cunha Francis?L.?Pazini Fabiana?K.?Ludka Julia?M.?Rosa ágatha?Oliveira Josiane?Budni Ana?B.?Ramos-Hryb Vicente?Lieberknecht Luis?E.?B.?Bettio Maria?D.?Martín-de-Saavedra Manuela?G.?López Carla?I.?Tasca Ana?Lúcia?S.?RodriguesEmail author 《Amino acids》2015,47(4):795-811
The modulation of N-methyl-D-aspartate receptor (NMDAR) and l-arginine/nitric oxide (NO) pathway is a therapeutic strategy for treating depression and neurologic disorders that involves excitotoxicity. Literature data have reported that creatine exhibits antidepressant and neuroprotective effects, but the implication of NMDAR and l-arginine/nitric oxide (NO) pathway in these effects is not established. This study evaluated the influence of pharmacological agents that modulate NMDAR/l-arginine-NO pathway in the anti-immobility effect of creatine in the tail suspension test (TST) in mice. The NOx levels and cellular viability in hippocampal and cerebrocortical slices of creatine-treated mice were also evaluated. The anti-immobility effect of creatine (10 mg/kg, po) in the TST was abolished by NMDA (0.1 pmol/mouse, icv), d-serine (30 µg/mouse, icv, glycine-site NMDAR agonist), arcaine (1 mg/kg, ip, polyamine site NMDAR antagonist), l-arginine (750 mg/kg, ip, NO precursor), SNAP (25 μg/mouse, icv, NO donor), L-NAME (175 mg/kg, ip, non-selective NOS inhibitor) or 7-nitroindazole (50 mg/kg, ip, neuronal NOS inhibitor), but not by DNQX (2.5 µg/mouse, icv, AMPA receptor antagonist). The combined administration of sub-effective doses of creatine (0.01 mg/kg, po) and NMDAR antagonists MK-801 (0.001 mg/kg, po) or ketamine (0.1 mg/kg, ip) reduced immobility time in the TST. Creatine (10 mg/kg, po) increased cellular viability in hippocampal and cerebrocortical slices and enhanced hippocampal and cerebrocortical NO x levels, an effect potentiated by l-arginine or SNAP and abolished by 7-nitroindazole or L-NAME. In conclusion, the anti-immobility effect of creatine in the TST involves NMDAR inhibition and enhancement of NO levels accompanied by an increase in neural viability. 相似文献
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Manuella P. Kaster Josiane Budni Marta Gazal Mauricio P. Cunha Adair R. S. Santos Ana Lúcia S. Rodrigues 《Purinergic signalling》2013,9(3):481-486
Inosine is an endogenous purine nucleoside, which is formed during the breakdown of adenosine. The adenosinergic system was already described as capable of modulating mood in preclinical models; we now explored the effects of inosine in two predictive models of depression: the forced swim test (FST) and tail suspension test (TST). Mice treated with inosine displayed higher anti-immobility in the FST (5 and 50 mg/kg, intraperitoneal route (i.p.)) and in the TST (1 and 10 mg/kg, i.p.) when compared to vehicle-treated groups. These antidepressant-like effects started 30 min and lasted for 2 h after intraperitoneal administration of inosine and were not accompanied by any changes in the ambulatory activity in the open-field test. Both adenosine A1 and A2A receptor antagonists prevented the antidepressant-like effect of inosine in the FST. In addition, the administration of an adenosine deaminase inhibitor (1 and 10 mg/kg, i.p.) also caused an antidepressant-like effect in the FST. These results indicate that inosine possesses an antidepressant-like effect in the FST and TST probably through the activation of adenosine A1 and A2A receptors, further reinforcing the potential of targeting the purinergic system to the management of mood disorders. 相似文献
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ConBr,a lectin from Canavalia brasiliensis seeds,modulates signaling pathways and increases BDNF expression probably via a glycosylated target 下载免费PDF全文
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Dal-Cim T Molz S Egea J Parada E Romero A Budni J Martín de Saavedra MD Barrio LD Tasca CI López MG 《Neurochemistry international》2012,61(3):397-404
Mitochondrial perturbation and oxidative stress are key factors in neuronal vulnerability in several neurodegenerative diseases or during brain ischemia. Here we have investigated the protective mechanism of action of guanosine, the guanine nucleoside, in a human neuroblastoma cell line, SH-SY5Y, subjected to mitochondrial oxidative stress. Blockade of mitochondrial complexes I and V with rotenone plus oligomycin (Rot/oligo) caused a significant decrease in cell viability and an increase in ROS production. Guanosine that the protective effect of guanosine incubated concomitantly with Rot/oligo abolished Rot/oligo-induced cell death and ROS production in a concentration dependent manner; maximum protection was achieved at the concentration of 1mM. The cytoprotective effect afforded by guanosine was abolished by adenosine A(1) or A(2A) receptor antagonists (DPCPX or ZM241385, respectively), or by a large (big) conductance Ca(2+)-activated K(+) channel (BK) blocker (charybdotoxin). Evaluation of signaling pathways showed that the protective effect of guanosine was not abolished by a MEK inhibitor (PD98059), by a p38(MAPK) inhibitor (SB203580), or by a PKC inhibitor (cheleritrine). However, when blocking the PI3K/Akt pathway with LY294002, the neuroprotective effect of guanosine was abolished. Guanosine increased Akt and p-Ser-9-GSK-3β phosphorylation confirming this pathway plays a key role in guanosine's neuroprotective effect. Guanosine induced the antioxidant enzyme heme oxygenase-1 (HO-1) expression. The protective effects of guanosine were prevented by heme oxygenase-1 inhibitor, SnPP. Moreover, bilirubin, an antioxidant and physiologic product of HO-1, is protective against mitochondrial oxidative stress. In conclusion, our results show that guanosine can afford protection against mitochondrial oxidative stress by a signaling pathway that implicates PI3K/Akt/GSK-3β proteins and induction of the antioxidant enzyme HO-1. 相似文献
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Budni P de Lima MN Polydoro M Moreira JC Schroder N Dal-Pizzol F 《Neurochemical research》2007,32(6):965-972
Increased levels of iron in specific brain regions have been reported in neurodegenerative disorders. It has been postulated
that iron exerts its deleterious effects on the nervous system by inducing oxidative damage. In a previous study, we have
shown that iron administered during a particular period of the neonatal life induces oxidative damage in brain regions in
adult rats. The aim of the present study was to evaluate the possible protective effect of selegiline, a monoamino-oxidase
B (MAO-B) inhibitor used in pharmacotherapy of Parkinson’s disease, against iron-induced oxidative stress in the brain. Results
have shown that selegiline (1.0 and 10.0 mg/kg), when administered early in life was able to protect the substantia nigra
as well as the hippocampus against iron-induced oxidative stress, without affecting striatum. When selegiline (10.0 mg/kg)
was administered in the adult life to iron-treated rats, oxidative stress was reduced only in the substantia nigra. 相似文献
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