IMIBIO-SL   20937
INSTITUTO MULTIDISCIPLINARIO DE INVESTIGACIONES BIOLOGICAS DE SAN LUIS
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
AGING MODIFIES TEMPORAL PATTERNS OF OXIDATIVE STRESS AND PROINFLAMMATORY MARKERS IN THE RAT PREFRONTAL CORTEX
Autor/es:
PONCE, IVANA T.; DEVIA C; ANZULOVICH, AC; NAVIGATORE FONZO LORENA; KLUSCH E; CORIA LUCERO; FERNANDEZ G
Reunión:
Congreso; XXXVI Reunión Científica Anual de la Sociedad de Biología de Cuyo; 2018
Resumen:
Aging is often accompanied by a decline in cognitive function in conjunction with a variety of neurobiological changes, such as neuroinflammationand oxidative damage. The brain is vulnerable to oxidative damage because of its large amount of polyunsaturatedfatty acidsand relative deficiency inantioxidative defense mechanisms. Recent research has shown that theexpression of proinfammatory cytokines increases withaging in brain. Besides cognitive deficit, older personsshow alterations in their circadian rhythms.The objective of this work was to investigate the consequences of aging on 24h patterns of oxidative stress parameters (TBARS and protein carbonyls )as well as TNFα, BMAL1 and RORα protein levels, in the rat prefrontal cortex (PFC). Holtzman rats from young (3-month-old) and aged (22-month-old) groups were maintained under constantdarkness conditions, during 10 days before the experiment. Tissues samples were isolated every 6 h during a 24h period. TBAR?s levels were measured by a colorimetric assay and protein carbonyls by ELISA. Protein levels ofTNFα, BMAL1 and RORα were determined by immunoblotting. As expected, we observed an increase in the protein carbonyls levels in the PFC ofaged rats.We also found that lipoperoxidation as well as protein levels of TNFα, BMAL1 and RORα follow a robustcircadian rhythm in this tissue.Interestingly,aging abolishes the oscillation of endogenous circadian patterns oflipoperoxidation,TNFα, BMAL1 and RORαprotein levels.These findings may constitute, at least in part, the molecular basis of the relationship between TNF-mediated neuroinflammation and altered circadian rhythms of protein clock in aged individuals.