Abstract
We report herein a study of aging using in vitro and in vivo models. Glial fibrillary acidic protein and ferritin expression levels increased, and the levels of glutamate transporter 1 and transferrin receptor 1 decreased in aging mouse spinal cord and its astrocytes. Mitochondrial transmembrane potential in astrocytes decreased after 60 d of culture. Given the relationship between aging and loss of antioxidant tolerance capacity, we examined the expression of heme oxygenase 1 (HO1) and NAD(P)H/quinone oxidoreductase 1 (NQO1) in the old mouse astrocytes and spinal cord. Indeed, both antioxidant enzymes decreased there. Total nuclear factor E2-related factor 2, which governs basal and inducible expression of HO1 and NQO1, decreased significantly. Significantly, epigallocatechin gallate restored the Nrf2 activity.
MeSH terms
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Aging / metabolism*
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Animals
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Astrocytes / metabolism*
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Catechin / analogs & derivatives
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Catechin / pharmacology
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Cells, Cultured
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Excitatory Amino Acid Transporter 2 / metabolism
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Ferritins / metabolism
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Glial Fibrillary Acidic Protein / metabolism
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Heme Oxygenase-1 / metabolism
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Membrane Potential, Mitochondrial
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Mice
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Models, Animal
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NAD(P)H Dehydrogenase (Quinone)
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NADPH Dehydrogenase / metabolism
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NF-E2-Related Factor 2 / metabolism*
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Neuroprotective Agents / pharmacology
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Receptors, Transferrin / metabolism
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Spinal Cord / cytology
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Spinal Cord / metabolism*
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Time Factors
Substances
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Excitatory Amino Acid Transporter 2
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Glial Fibrillary Acidic Protein
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NF-E2-Related Factor 2
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Neuroprotective Agents
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Nfe2l2 protein, mouse
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Receptors, Transferrin
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Tfrc protein, mouse
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Catechin
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Ferritins
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epigallocatechin gallate
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Heme Oxygenase-1
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NAD(P)H Dehydrogenase (Quinone)
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Nqo1 protein, mouse
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NADPH Dehydrogenase