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Kawamoto,E.M.; Gleichmann,M.; Yshii,L.M.; Lima,L. de Sá; Mattson,M.P.; Scavone,C.. |
Wnt proteins are involved in tissue development and their signaling pathways play an important role during embryogenesis. Wnt signaling can promote cell survival, which is beneficial for neurons, but could also lead to tumor development in different tissues. The present study investigated the effects of a Wnt protein on the susceptibility of a neural tumor cell line (PC12 cells) to the cytotoxic compounds ferrous sulfate (10 mM), staurosporine (100 and 500 nM), 3-nitropropionic acid (5 mM), and amyloid β-peptide (Aβ25-35; 50 µM). Cells (1 x 10(6) cells/mL) were treated with the Wnt-3a recombinant peptide (200 ng/mL) for 24 h before exposure to toxic insults. The Wnt-3a protein partially protected PC12 cells, with a 6-15% increase in cell viability in the... |
Tipo: Info:eu-repo/semantics/article |
Palavras-chave: Wnt-3a; PC12 cells; Beta-catenin; NF-κB. |
Ano: 2012 |
URL: http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2012000100010 |
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Planeta,C.S.; Lepsch,L.B.; Alves,R.; Scavone,C.. |
Cocaine is a widely used drug and its abuse is associated with physical, psychiatric and social problems. Abnormalities in newborns have been demonstrated to be due to the toxic effects of cocaine during fetal development. The mechanism by which cocaine causes neurological damage is complex and involves interactions of the drug with several neurotransmitter systems, such as the increase of extracellular levels of dopamine and free radicals, and modulation of transcription factors. The aim of this review was to evaluate the importance of the dopaminergic system and the participation of inflammatory signaling in cocaine neurotoxicity. Our study showed that cocaine activates the transcription factors NF-κB and CREB, which regulate genes involved in cellular... |
Tipo: Info:eu-repo/semantics/article |
Palavras-chave: Cocaine; Apoptosis; NF-κB; CREB; BDNF; Neurotoxicity. |
Ano: 2013 |
URL: http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2013001100909 |
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Alba-Loureiro,T.C.; Munhoz,C.D.; Martins,J.O.; Cerchiaro,G.A.; Scavone,C.; Curi,R.; Sannomiya,P.. |
Neutrophils act as first-line-of-defense cells and the reduction of their functional activity contributes to the high susceptibilityto and severity of infections in diabetes mellitus. Clinical investigations in diabetic patients and experimental studies in diabetic rats and mice clearly demonstrated consistent defects of neutrophil chemotactic, phagocytic and microbicidal activities. Other alterations that have been reported to occur during inflammation in diabetes mellitus include: decreased microvascular responses to inflammatory mediators such as histamine and bradykinin, reduced protein leakage and edema formation, reduced mast cell degranulation, impairment of neutrophil adhesionto the endothelium and migration to the site of inflammation, production... |
Tipo: Info:eu-repo/semantics/article |
Palavras-chave: Neutrophils; Inflammation; Diabetes mellitus; Insulin; Metabolism and cellular function. |
Ano: 2007 |
URL: http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2007000800003 |
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Munhoz,C.D.; García-Bueno,B.; Madrigal,J.L.M.; Lepsch,L.B.; Scavone,C.; Leza,J.C.. |
Stress is triggered by numerous unexpected environmental, social or pathological stimuli occurring during the life of animals, including humans, which determine changes in all of their systems. Although acute stress is essential for survival, chronic, long-lasting stress can be detrimental. In this review, we present data supporting the hypothesis that stress-related events are characterized by modifications of oxidative/nitrosative pathways in the brain in response to the activation of inflammatory mediators. Recent findings indicate a key role for nitric oxide (NO) and an excess of pro-oxidants in various brain areas as responsible for both neuronal functional impairment and structural damage. Similarly, cyclooxygenase-2 (COX-2), another known source of... |
Tipo: Info:eu-repo/semantics/article |
Palavras-chave: Cyclooxygenase; Nitric oxide; PPARγ; Stress-induced neurodegeneration. |
Ano: 2008 |
URL: http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2008001200001 |
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