Tominaga K, Shibata S, Watanabe S
Department of Pharmacology, Faculty of Pharmaceutical Sciences, Kyushu University, Fukuoka, Japan.
Neurosci Lett. 1992 Sep 28;145(1):67-70. doi: 10.1016/0304-3940(92)90205-l.
The effects of adenosine (A) receptor agonists on ischemia-induced impairment of 2-deoxyglucose (2-DG) uptake by rat hippocampal slices was evaluated. Hippocampal slices were exposed to 20-min hypoxia + hypoglycemia (ischemia) and then returned to oxygenated and glucose-containing Krebs-Ringer solution for 6 h. Ischemia reduced 2-DG uptake in the hippocampal slices. The ischemia-induced reduction in 2-DG uptake was attenuated by pretreatment with A1 receptor agonists but not with A2 receptor agonists. 8-Phenyltheophylline, an A1 receptor antagonist, exacerbated the ischemia-induced decrease. The A1 receptor agonist-induced neuroprotective effect was blocked by co-treatment with 8-phenyltheophylline. The present study suggests that the A1 receptor-mediated function has a protective role in ischemia-induced decreases in glucose metabolism in hippocampal slices.
评估了腺苷（A）受体激动剂对缺血诱导的大鼠海马切片2-脱氧葡萄糖（2-DG）摄取受损的影响。将海马切片暴露于20分钟的缺氧+低血糖（缺血）状态，然后放回含氧气和葡萄糖的 Krebs-Ringer 溶液中6小时。缺血降低了海马切片中2-DG的摄取。用A1受体激动剂预处理可减轻缺血诱导的2-DG摄取减少，而用A2受体激动剂预处理则无此作用。A1受体拮抗剂8-苯基茶碱加剧了缺血诱导的降低。与8-苯基茶碱共同处理可阻断A1受体激动剂诱导的神经保护作用。本研究表明，A1受体介导的功能对缺血诱导的海马切片葡萄糖代谢降低具有保护作用。
