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Genistein And Estradiol Increase Anti-inflammatory Proteins In Astrocytes In Culture | 12490
ISSN: 2161-0460

Journal of Alzheimers Disease & Parkinsonism
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Genistein and estradiol increase anti-inflammatory proteins in astrocytes in culture

International Conference on Psychology, Autism and Alzheimers Disease

Correa Pablo

ScientificTracks Abstracts: J Alzheimers Dis Parkinsonism

DOI: 10.4172/2161-0460.S1.002

Abstract
Estrogens and phytoestrogen such as genistein, have been demonstrated to promote anti-oxidant and anti-inflammatory properties after A? cell death induction. We previously published that genistein can induced anti-inflammatory proteins such as PPAR-? and decrease IL-1 and TNF-? (proinflammatory proteins) producing a decrease in apoptosis in astrocytes in primary culture. To know the molecular mechanism of action, we look for protein expression of MAPkinases, such as ERK, JUN and p-38 and also we determine NFkB and AP-1 protein induction in astrocytes in primary culture. Our data indicate that A? compound can trigger signal transduction pathways linked to apoptosis, such as caspases, p53, and bcl-2 genes. This programmed-cell death may be considered actually one of the important targets in a preventive approach against Alzheimer?s disease. How estrogens and phytoestrogens do regulate and control the intracellular signaling cascades considered as relevant targets in neurodegenerative preventive approach remains to be elucidated. The results suggest that in neural cells, blocking the cellular signal transduction might trigger the induction of apoptosis and also estrogens can regulate signaling cascades to stop conversion of a normal cell to an affected one by compounds in Alzheimer?s disease.
Biography
Estrogens and phytoestrogen such as genistein, have been demonstrated to promote anti-oxidant and anti-inflammatory properties after A? cell death induction. We previously published that genistein can induced anti-inflammatory proteins such as PPAR-? and decrease IL-1 and TNF-? (proinflammatory proteins) producing a decrease in apoptosis in astrocytes in primary culture. To know the molecular mechanism of action, we look for protein expression of MAPkinases, such as ERK, JUN and p-38 and also we determine NFkB and AP-1 protein induction in astrocytes in primary culture. Our data indicate that A? compound can trigger signal transduction pathways linked to apoptosis, such as caspases, p53, and bcl-2 genes. This programmed-cell death may be considered actually one of the important targets in a preventive approach against Alzheimer?s disease. How estrogens and phytoestrogens do regulate and control the intracellular signaling cascades considered as relevant targets in neurodegenerative preventive approach remains to be elucidated. The results suggest that in neural cells, blocking the cellular signal transduction might trigger the induction of apoptosis and also estrogens can regulate signaling cascades to stop conversion of a normal cell to an affected one by compounds in Alzheimer?s disease.
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