Asanuma M, Asanuma S N, Gómez-Vargas M, Yamamoto M, Ogawa N
Department of Neuroscience, Okayama University Medical School, Japan.
Neurosci Lett. 1997 Apr 4;225(2):109-12. doi: 10.1016/s0304-3940(97)00204-8.
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.
缺血诱导的海马区毒蕈碱型乙酰胆碱受体迟发性减少（LORMAR）在沙土鼠短暂性前脑缺血后最晚7天开始出现，但早于CA1区神经元死亡的完成。我们之前报道过，缺血后给予环孢素A可通过抑制星形胶质细胞和小胶质细胞的激活来预防LORMAR。在本研究中，我们发现，在5分钟短暂缺血后14天和21天，慢性缺血后给予非甾体抗炎药酮洛芬（5毫克/千克，皮下注射，每天两次，共14天）可显著降低LORMAR。酮洛芬对LORMAR的这种保护作用表明，非甾体抗炎药在治疗作为脑缺血后遗症的LORMAR方面具有临床疗效。
