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PPAR-α Expression Inversely Correlates with Inflammatory Cytokines IL-1β and TNF-α in Aging Rats

Gelinas DS, McLaurin J2005Neurochemical ResearchJournal Article
10.1007/s11064-005-8341-yPubMed
Endocrine (ADH/ACTH/MSH)Immune/InnateNeurological

Abstract

Dehydroepiandrosterone (DHEAS) was given the name "fountain of youth" in reference to its beneficial properties in memory, cognition and aging. Cultured cell studies showed that DHEAS may mediate its action by counteracting aging-associated inflammation via PPAR-alpha activation. In the present study, we demonstrated an age-dependent increase in IL-1beta and TNF-alpha expression in the brain and the spleen of aging rats, while PPAR-alpha expression was decreased in the spleen of 18 month-old rats. Oral treatment with DHEAS increased PPAR-alpha mRNA in 3 month-old rats and decreased PPAR-alpha protein expression in 18 month-old rats in the spleen. In contrast, DHEAS did not alter cytokine expression in spleen and brain of the three age groups. These findings underline a differential role for DHEAS in PPAR-alpha expression that is age-dependent, and also, that beneficial effects of DHEAS on cognitive function are unlikely mediated by a decrease in cytokine expression.

Key Biomarkers

DHEASIL-1βPPAR-alphaTNF-α

Symptom Clusters

Aging-associated inflammationCognitive decline

References (3)

  • Peroxisome Proliferator-activated Receptor α Negatively Regulates the Vascular Inflammatory Gene Response by Negative Cross-talk with Transcription Factors NF-κB and AP-1Journal of Biological Chemistry · 1999
  • PPAR-γ agonists inhibit production of monocyte inflammatory cytokinesNature · 1998
  • The peroxisome proliferator-activated receptor-γ is a negative regulator of macrophage activationNature · 1998

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