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首页> 外文期刊>CNS neuroscience & therapeutics. >Transient Lack of Glucose but not Osub2/sub is Involved in Ischemic Postconditioning‐Induced Neuroprotection
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Transient Lack of Glucose but not Osub2/sub is Involved in Ischemic Postconditioning‐Induced Neuroprotection

机译：短暂缺乏葡萄糖而不是O 2 参与缺血后适应诱导的神经保护

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Summary Aim Cerebral ischemic postconditioning has emerged recently as a kind of endogenous strategy for neuroprotection. We set out to test whether hypoxia or glucose deprivation ( GD ) would substitute for ischemia in postconditioning. Methods Adult male C 57 BL /6 J mice were treated with postconditioning evoked by ischemia (bilateral common carotid arteries occlusion) or hypoxia (8% O 2) after 45‐min middle cerebral arterial occlusion. Corticostriatal slices from mice were subjected to 1‐min oxygen‐glucose deprivation ( OGD ), GD , or oxygen deprivation ( OD ) postconditioning at 5 min after 15‐min OGD . Results Hypoxic postconditioning did not decrease infarct volume or improve neurologic function at 24 h after reperfusion, while ischemic postconditioning did. Similarly, OGD and GD but not OD postconditioning attenuated the OGD /reperfusion‐induced injury in corticostriatal slices. The effective duration of low‐glucose (1 mmol/L) postconditioning was longer than that of OGD postconditioning. Moreover, OGD and GD but not OD postconditioning reversed the changes of glutamate, GABA , glutamate transporter‐1 protein expression, and glutamine synthetase activity induced by OGD /reperfusion. Conclusions These results suggest that the transient lack of glucose but not oxygen plays a key role in ischemic postconditioning‐induced neuroprotection, at least partly by regulating glutamate metabolism. Low‐glucose postconditioning might be a clinically safe and feasible therapeutic approach against cerebral ischemia/reperfusion injury.
机译：总结目的缺血性后处理是近来出现的一种内源性神经保护策略。我们着手测试缺氧或葡萄糖剥夺（GD）是否可以替代后处理中的局部缺血。方法成年雄性C 57 BL / 6 J小鼠在大脑中动脉闭塞45分钟后进行缺血（双侧颈总动脉闭塞）或缺氧（8％O 2）诱发的后处理。在15分钟OGD后的5分钟内，对小鼠的皮层皮质切片进行1分钟的氧葡萄糖剥夺（OGD），GD或氧剥夺（OD）后处理。结果低氧后处理在再灌注后24 h并没有减少梗塞体积或改善神经功能，而缺血后处理却没有。同样，OGD和GD，但OD后处理则不能减弱OGD /皮层皮质切片中再灌注引起的损伤。低血糖（1 mmol / L）后处理的有效时间长于OGD后处理的有效时间。此外，OGD和GD而不是OD后处理可以逆转OGD /再灌注诱导的谷氨酸，GABA，谷氨酸转运蛋白-1蛋白表达和谷氨酰胺合成酶活性的变化。结论这些结果表明，短暂缺乏葡萄糖而不是氧气在缺血后处理诱导的神经保护中起关键作用，至少部分是通过调节谷氨酸代谢。低血糖后处理可能是一种针对脑缺血/再灌注损伤的临床安全可行的治疗方法。

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