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Signaling function of Na,K-ATPase induced by ouabain against LPS as an inflammation model in hippocampus

Paula Fernanda Kinoshita1, Lidia Mitiko Yshii2, Andrea Rodrigues Vasconcelos3

  • 1Molecular Neuropharmacology Laboratory, Department of Pharmacology, Institute of Biomedical Science, University of São Paulo, 05508-900, São Paulo, Brazil. paula.f.kinoshita@gmail.com.

Journal of Neuroinflammation
|January 1, 2015
PubMed
Abstract

Insights

Low-dose ouabain (OUA) significantly reduces inflammation and apoptosis in the rat hippocampus following lipopolysaccharide (LPS) exposure. This neuroprotective effect involves inhibiting NF-κB activation and reducing glial fibrillary acidic protein (GFAP) induction.

Area of Science:

  • Neuroscience
  • Pharmacology
  • Inflammation Research

Background:

  • Ouabain (OUA) is an endogenous hormone with known anti-inflammatory properties.
  • Lipopolysaccharide (LPS) is a potent inducer of systemic inflammation via toll-like receptor 4 activation.
  • Low-dose OUA may offer protection against LPS-induced inflammatory insults.

Purpose of the Study:

  • To investigate the anti-inflammatory and neuroprotective effects of low-dose OUA in an LPS-induced inflammation model in rats.
  • To elucidate the underlying molecular mechanisms, including NF-κB pathway and apoptosis markers.

Main Methods:

  • Adult male Wistar rats were pretreated with OUA or saline before LPS or saline injection.
  • Measurements included arterial blood pressure, Na,K-ATPase activity, cytokine mRNA, apoptosis proteins, NF-κB activation, BDNF, corticosterone, and TNF-α.
  • Specific assessments focused on hippocampal and serum inflammatory markers and cellular changes.

Main Results:

  • OUA pretreatment reduced hippocampal pro-inflammatory cytokine mRNA (iNOS, IL-1β) but not serum levels.
  • OUA inhibited LPS-induced NF-κB activation by preventing RELA nuclear translocation and decreasing IKB levels in the hippocampus.
  • OUA reversed LPS-induced GFAP activation and reduced the Bax/Bcl2 ratio, indicating anti-apoptotic effects in the hippocampus.

Conclusions:

  • Low-dose OUA exerts significant anti-inflammatory effects in the rat hippocampus.
  • The protective mechanism involves the inhibition of NF-κB signaling and reduction of LPS-induced neuroinflammation and apoptosis.
  • OUA's effects on GFAP induction in the dentate gyrus suggest a role in modulating neurogenesis-related inflammation.

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