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• W2018746851 abstract "Proton pump inhibitors (PPIs) are known to possess anti-inflammatory properties. Inflammatory processes, including astrocytic activation, are implicated in the pathogenesis of different neurodegenerative diseases. Our recent study has indicated that interferon (IFN)-γ-induced astrocytic neurotoxicity is mediated, at least in part, by phosphorylation of signal transducer and activator of transcription (STAT) 3. We therefore studied the effects of PPIs on IFN-γ-induced neurotoxicity and STAT3 activation of human astrocytes. Both lansoprazole (LPZ) and omeprazole (OPZ) significantly attenuated IFN-γ-induced neurotoxicity of human astrocytes and astrocytoma cells. These drugs inhibited IFN-γ-induced phosphorylation of STAT 3, but not STAT1. We found that LPZ significantly reduced secretion of IFN-γ-inducible T cell α chemoattractant from IFN-γ-activated astrocytes. Neither LPZ nor OPZ suppressed expression of intercellular adhesion molecule-1 by IFN-γ-activated astrocytes. These results suggest that PPIs attenuate IFN-γ-induced neurotoxicity of human astrocytes through inhibition of the STAT3 signaling pathway. PPIs that possess antineurotoxic properties may be a useful treatment option for Alzheimer's disease and other neuroinflammatory disorders associated with activated astrocytes. © 2011 Wiley-Liss, Inc." @default.
• W2018746851 created "2016-06-24" @default.
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• W2018746851 date "2011-02-28" @default.
• W2018746851 modified "2023-09-23" @default.
• W2018746851 title "Proton pump inhibitors reduce interferon-γ-induced neurotoxicity and STAT3 phosphorylation of human astrocytes" @default.
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• W2018746851 doi "https://doi.org/10.1002/glia.21157" @default.
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