These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Non-steroidal anti-inflammatory drugs protect amyloid beta protein-induced increase in the intracellular Cl- concentration in cultured rat hippocampal neurons.
    Author: Iwata R, Kitagawa K, Zhang NY, Wu B, Inagaki C.
    Journal: Neurosci Lett; 2004 Sep 02; 367(2):156-9. PubMed ID: 15331142.
    Abstract:
    Long-term use of non-steroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen reportedly decrease a risk for the progression of Alzheimer's disease (AD), whose mechanisms are still controversial. We previously reported that pathophysiological concentrations (1-10 nM) of amyloid beta proteins (Abetas) increased intracellular Cl- concentration ([Cl-]i) and aggravated glutamate neurotoxicity in the rat brain neuronal culture. In this study, we examined the effects of therapeutic concentrations of ibuprofen and other drugs with cyclo-oxygenase (COX)-1 and/or COX-2 inhibiting activities on 10 nM Abeta25-35-induced changes in cultured rat hippocampal neurons. Ibuprofen (10-100 microM) dose-dependently inhibited the Abeta25-35-induced increase in [Cl-]i in pyramidal cell-like neurons. Not only ibuprofen, aspirin (100 microM), indomethacin (50 microM), and selective COX-1 or COX-2 inhibitor (10 nM ketrolac or 2 microM NS398) also blocked the Abeta-induced increase in neuronal [Cl-]i, though such effects of COX-2 preferring drugs were limited in aggregated Abeta-induced changes. Further, ibuprofen as well as selective COX-1 or COX-2 inhibitor reduced Abeta-induced aggravation of glutamate toxicity as assessed by cell viability. These findings suggest that NSAIDs protect neurons from Abeta-induced degeneration via inhibition of neuronal COX-1 as well as COX-2.
    [Abstract] [Full Text] [Related] [New Search]