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  • Title: Suppression of lipopolysaccharide-induced impairment of active avoidance and interleukin-6-induced increase of prostaglandin E2 release in rats by indometacin.
    Author: Ma TC, Zhu XZ.
    Journal: Arzneimittelforschung; 1997 May; 47(5):595-7. PubMed ID: 9205771.
    Abstract:
    The effects of indometacin (CAS 53-86-1) on lipopolysaccharide-induced impairment of active avoidance and on interleukin-6-induced increase of prostaglandin E2 release were investigated in rats. In the experiment on acquisition and retention of one-way active avoidance in a shuttle box model, bilateral infusion of lipopolysaccharides (LPS) into the hippocampus, 1 microgram per side, resulted in a significant impairment both in acquisition and retention by prolonging the latency of avoidance in training and testing. In the meantime, intraperitoneal injection of indometacin 10 mg/kg daily for 7 days, improved the LPS-induced amnesia especially in the testing by shortening the latency from 2.3 to 1.7 s (p < 0.05). In the in vivo microdialysis study in anesthetized rats, intrahippocampal infusion of 80 ng interleukin-6 (IL-6) markedly increased prostaglandin E2 (PGE2) release into hippocampal dialysates which started at 2 h post administration. Perfusion of indometacin (0.3 mol/l) into the hippocampus for 1 h obviously suppressed the IL-6-induced PGE2 response. These findings provide experimental evidence that--assuming that central inflammation may be involved with Alzheimer's disease a non-steroidal anti-inflammatory drug may be used in the treatment of Alzheimer's disease.
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