|
|
|
|
|
| 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 |
| |
|
|
| 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 |
| |
|
|
|
