Navegando por Palavras-chave "p38"

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    Aerobic exercise reduces hippocampal ERK and p38 activation and improves memory of middle-aged rats
    (Wiley, 2017) Cardoso, Fabrizio dos Santos; Franca, Erivelton Fernandes; Serra, Fernando Tadeu; Victorino, Angelica Begatti [UNIFESP]; de Almeida, Alexandre Aparecido [UNIFESP]; Fernandes, Jansen [UNIFESP]; Cabral, Francisco Romero; Venancio, Daniel Paulino; Arida, Ricardo Mario [UNIFESP]; da Silva, Sergio Gomes
    Aging is often accompanied by cognitive decline, memory impairment, and an increased susceptibility to neurodegenerative disorders. Although the physiological processes of aging are not fully understood, these age-related changes have been interpreted by means of various cellular and molecular theories. Among these theories, alterations in the intracellular signaling pathways associated with cell growth, proliferation, and survival have been highlighted. Based on these observations and on recent evidence showing the beneficial effects of exercise on cognitive function in the elderly, we investigated the cell signaling pathways in the hippocampal formation of middle-aged rats (18months old) submitted to treadmill exercise over 10 days. To do this, we evaluated the hippocampal activation of intracellular signaling proteins linked to cell growth, proliferation, and survival, such as Akt, mTOR, p70S6K, ERK, CREB, and p38. We also explored the cognitive performance (inhibitory avoidance) of middle-aged rats. It was found that physical exercise reduces ERK and p38 activation in the hippocampal formation of aged rats, when compared to the control group. The hippocampal activation and expression of Akt, mTOR, p70S6K, and CREB were not statistically different between the groups. It was also observed that aged rats from the exercise group exhibited better cognitive performance in the inhibitory avoidance task (aversive memory) than aged rats from the control group. Our results indicate that physical exercise reduces intracellular signaling pathways linked to inflammation and cell death (i.e., ERK and p38) and improves memory in middle-aged rats.
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    Differential expression of toll-like receptor signaling cascades in LPS-tolerant human peripheral blood mononuclear cells
    (Elsevier B.V., 2011-03-01) Mendes, Marialice Erdelyi [UNIFESP]; Baggio-Zappia, Giovana Lotici [UNIFESP]; Colo Brunialti, Milena Karina [UNIFESP]; Fernandes, Maria da Luz [UNIFESP]; Rapozo, Marjorie Marini [UNIFESP]; Salomao, Reinaldo [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)
    Pre-exposure to low doses of LPS induces resistance to a lethal challenge, a phenomenon known as endotoxin tolerance. in this study, tolerance was induced in human PBMC by culturing cells with 1 ng/mL LPS for 48 h. Cells were subsequently challenged with 100 ng/mL LPS for 2, 6 and 24 h, and the expression of 84 genes encoding proteins involved in the TLR signaling pathway was evaluated at each time point by PCR array. LPS pretreatment did not modulate the expression of TLR4 and CD14 on the surface of monocytes. A gene was defined as tolerized when LPS pretreatment reversed the effect of LPS challenge on the expression of the gene or as non-tolerized when LPS pretreatment did not reverse the effects of LPS challenge. We observed impaired signal transduction through the NF-kappa B, JNK, ERK and TRIF pathways, whereas expression of p38 pathway-related genes was preserved in LPS-tolerant cells. These results show a distinct regulation of the TLR pathway cascades during tolerance; this may account for the differential gene expression of some inflammatory mediators, such as up-regulation of IL-10 and COX2 as well as down-regulation of INF-alpha and IL-12. Depending on the effect of LPS-induced gene up-regulation or down-regulation, tolerance, as a reversion of such LPS effects, may result in repression or induction of gene expression. (C) 2010 Elsevier GmbH. All rights reserved.