TY - JOUR
T1 - Ketoprofen, a non-steroidal anti-inflammatory drug prevents the late-onset reduction of muscarinic receptors in gerbil hippocampus after transient forebrain ischemia
AU - Asanuma, Masato
AU - Asanuma, Sakiko N.
AU - Gómez-Vargas, Marvin
AU - Yamamoto, Mitsutoshi
AU - Ogawa, Norio
N1 - Funding Information:
This work was supported in part by Priority Areas and Scientific Research from the Japanese Ministry of Education, Science, Sports and Culture, and Grants-in-Aid for Scientific Research from the Research Committee on CNS Degenerative Diseases and Research Projects on Aging and Health from the Japanese Ministry of Health and Welfare.
PY - 1997/4/4
Y1 - 1997/4/4
N2 - 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 the 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.
AB - 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 the 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.
KW - Hippocampus
KW - Ketoprofen
KW - Late-onset damage
KW - Muscarinic acetylcholine receptor
KW - Non-steroidal anti-infalmmatory drug (NSAID)
KW - Transient forebrain ischemia
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U2 - 10.1016/S0304-3940(97)00204-8
DO - 10.1016/S0304-3940(97)00204-8
M3 - Article
C2 - 9147386
AN - SCOPUS:0031552371
SN - 0304-3940
VL - 225
SP - 109
EP - 112
JO - Neuroscience Letters
JF - Neuroscience Letters
IS - 2
ER -