Ketoprofen, a non-steroidal anti-inflammatory drug prevents the late-onset reduction of muscarinic receptors in gerbil hippocampus after transient forebrain ischemia.
Ischemia-induced hippocampal late-onset reduction of muscarinic acetylcholine receptors (LORMAR) begins as late as 7 days after transient forebrain ischemia in the gerbil, but it precedes to completion of neuronal death in the CA1 region. We previously reported that post-ischemic administration of cyclosporin A prevented LORMAR with suppression of astroglial and microglial activation. In the present study, we showed that the chronic post-ischemic administration of a non-steroidal anti-inflammatory drug, ketoprofen (5 mg/kg, subcutaneously, twice a day for 14 days) significantly reduced LORMAR both 14 days and 21 days after 5-min transient ischemia. This protective effect of ketoprofen against LORMAR suggests that the non-steroidal anti-inflammatory drugs is clinically efficacious in the treatment of LORMAR, a sequela of cerebral ischemia.
Asanuma
M
M
Department of Neuroscience, Okayama University Medical School, Japan.
Asanuma
S N
SN
Gómez-Vargas
M
M
Yamamoto
M
M
Ogawa
N
N
D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology*; D002545:Brain Ischemia / Q000188:drug therapy*; D005849:Gerbillinae; D006624:Hippocampus / Q000187:drug effects*; D007660:Ketoprofen / Q000494:pharmacology*; D008297:Male; D016548:Prosencephalon / Q000187:drug effects*; D011976:Receptors, Muscarinic / Q000187:drug effects*; D013997:Time Factors
D000894:Anti-Inflammatory Agents, Non-Steroidal; D011976:Receptors, Muscarinic; D007660:Ketoprofen