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中文摘要：
丝氨酸-苏氨酸蛋白激酶（AKT）被视为缺血缺氧中减轻神经细胞损伤的主要信号转导蛋白。糖原合成酶激酶3（GSK-3）是AKT下游的重要蛋白,在脑缺血缺氧损伤中发挥促凋亡作用。脑缺血缺氧损伤后,AKT磷酸化后激活,继而使GSK-3失活,发挥脑保护作用。该信号通路也参与各种化学制剂对脑缺血的保护机制。GSK-3抑制剂的研究和运用可能为缺血缺氧性脑损伤的临床治疗提供新的理论依据。
英文摘要：
Serine/threonine protein kinase AKT is regarded as a key signal transduction protein which alleviates hypoxic-ischemic brain injury.Glycogen synthase kinase 3（GSK-3）,one of the downstream signaling molecules of AKT,plays a role in promoting apoptotic signaling pathway.After phosphorylation,AKT can inactivate GSK-3 and thus protect brains from ischemic hypoxic injury.ATK-GSK3 pathway is involved in neural protective effects of various chemical agents under the stimulation of hypoxic-ischemia.Therefore,studies of inhibitors of GSK3 might provide novel therapeutic strategies for hypoxia-ischemic brain injury in clinic.
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