Bruer U, Weih M K, Isaev N K, Meisel A, Ruscher K, Bergk A, Trendelenburg G, Wiegand F, Victorov I V, Dirnagl U
Department of Neurology, Charité Hospital, Humboldt University, Berlin, Germany.
FEBS Lett. 1997 Sep 1;414(1):117-21. doi: 10.1016/s0014-5793(97)00954-x.
Sublethal ischemia leads to increased tolerance against subsequent prolonged cerebral ischemia in vivo. In the present study we modeled preconditioning mechanisms in a neuronal-enriched culture. Damage was significantly reduced (up to 72%) with 1.5 h of oxygen-glucose deprivation 48-72 h before 3 h oxygen-glucose deprivation. Tolerance was also elicited by Na+-K+-ATPase inhibition. No damage was observed when astroglial or endothelial cells were exposed to hypoxia for 3 and 6 h, respectively. We conclude that hypoxic preconditioning is a robust neuronal phenomenon in vitro with a similar temporal pattern and selective cellular vulnerability as the ischemic tolerance phenomenon shown in vivo.
亚致死性缺血可导致体内对随后延长的脑缺血的耐受性增加。在本研究中，我们在富含神经元的培养物中模拟预处理机制。在3小时氧糖剥夺前48 - 72小时进行1.5小时的氧糖剥夺，损伤显著减少（高达72%）。钠钾ATP酶抑制也可引发耐受性。当星形胶质细胞或内皮细胞分别暴露于缺氧3小时和6小时时，未观察到损伤。我们得出结论，低氧预处理在体外是一种强大的神经元现象，其时间模式和选择性细胞易损性与体内显示的缺血耐受现象相似。
