The peroxisome proliferator phenylbutyric acid (PBA) protects astrocytes from ts1 MoMuLV-induced oxidative cell death

Na Liu, Wenan Qiang, Xianghong Kuang, Philippe Thuillier, William S. Lynn, Paul K.Y. Wong

Research output: Contribution to journalArticle

24 Scopus citations

Abstract

Oxidative stress is involved in the pathogenesis of several neurodegenerative diseases, including Parkinson's disease, Alzheimer's disease, and HIV neuroAIDS. In this study, we have investigated an agent, phenylbutyric acid, that ameliorates cell death in murine astrocytes infected with ts1 MoMuLV (ts1). Phenylbutyric acid, an aromatic short chain fatty acid, was shown to prevent the loss of catalase that occurs in ts1 infected astrocytes, and to prevent ts1-mediated cell death. Cell cotransfection studies demonstrated that phenylbutyric acid activates peroxisome proliferator receptors (PPARs) in astrocytes, and binds to the peroxisome proliferator-activated receptors α and γ. This observation suggests that the effects of PBA may be mediated by PPARs in astrocytes. Phenylbutyric acid also maintained catalase protein levels in brain of ts1-infected mice, and delayed the hindlimb paralysis caused by ts1 infection. Because PBA activates peroxisome proliferator-activated receptors and prevents loss of catalase, we suggest that ts1-induced oxidative stress in infected astrocytes that is alleviated by PBA is mediated via PPARα and/or PPARγ.

Original languageEnglish (US)
Pages (from-to)318-325
Number of pages8
JournalJournal of neurovirology
Volume8
Issue number4
DOIs
StatePublished - Aug 1 2002

Keywords

  • Catalase
  • Peroxisome proliferator-activated receptors
  • Phenylbutyric acid
  • Retrovirus-induced neurodegeneration

ASJC Scopus subject areas

  • Neurology
  • Clinical Neurology
  • Cellular and Molecular Neuroscience
  • Virology

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