Monopoli A, Lozza G, Forlani A, Mattavelli A, Ongini E
Schering-Plough Research Institute, San Raffaele Science Park, Milan, Italy.
Neuroreport. 1998 Dec 1;9(17):3955-9. doi: 10.1097/00001756-199812010-00034.
Blockade of adenosine receptors can reduce cerebral infarct size in the model of global ischaemia. Using the potent and selective A2A adenosine receptor antagonist, SCH 58261, we assessed whether A2A receptors are involved in the neuronal damage following focal cerebral ischaemia as induced by occluding the left middle cerebral artery. SCH 58261 (0.01 mg/kg either i.p. or i.v.) administered to normotensive rats 10 min after ischaemia markedly reduced cortical infarct volume as measured 24 h later (30% vs controls, p < 0.05). Similar effects were observed when SCH 58261 (0.01 mg/kg, i.p.) was administered to hypertensive rats (28% infarct volume reduction vs controls, p < 0.05). Neuroprotective properties of SCH 58261 administered after ischaemia indicate that blockade of A2A adenosine receptors is a potentially useful biological target for the reduction of brain injury.
在全脑缺血模型中，腺苷受体阻断可减小脑梗死面积。使用强效且选择性的A2A腺苷受体拮抗剂SCH 58261，我们评估了A2A受体是否参与了因阻断左大脑中动脉诱导的局灶性脑缺血后的神经元损伤。在缺血10分钟后给正常血压大鼠腹腔注射或静脉注射SCH 58261（0.01mg/kg），24小时后测量发现皮质梗死体积显著减小（与对照组相比减少30%，p<0.05）。当给高血压大鼠腹腔注射SCH 58261（0.01mg/kg）时也观察到了类似效果（梗死体积比对照组减少28%，p<0.05）。缺血后给予SCH 58261的神经保护特性表明，阻断A2A腺苷受体是减少脑损伤的一个潜在有用的生物学靶点。
