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核心技术专利：CN118964589B侵权必究

核心技术专利：CN118964589B侵权必究

Peruche B, Krieglstein J

Institut für Pharmakologie und Toxikologie, Fachbereich Pharmazie und Lebensmittelchemie, Philipps-Universität Marburg, Lahn, Germany.

Prog Neuropsychopharmacol Biol Psychiatry. 1993 Jan;17(1):21-70. doi: 10.1016/0278-5846(93)90032-n.

Oxygen and energy deficits induces a cascade of pathological processes which lead to neuronal dysfunction and cell death. 2. The pathogenesis of ischemia-induced neuronal damage includes a disturbed calcium homeostasis, an excessive release of EAA and an enhanced formation of free oxygen radicals. 3. Calcium antagonists inhibit Ca2+ influx into the neuronal cell via VSCC. 4. Glutamate antagonists reduce intracellular Ca2+ concentration by inactivation of NMDA receptor-associated calcium channels (NMDA antagonists) or AMPA/quisqualate receptor-linked sodium channels (non-NMDA antagonists). 5. Furthermore, oxygen radical scavengers can avoid neuronal damage. 6. Agonists of the adenosinergic and serotonergic transmitter systems contribute to neuroprotection by hyperpolarization of the neuronal membrane due to an increase of K+ permeability.

氧和能量缺乏会引发一系列病理过程，进而导致神经元功能障碍和细胞死亡。2. 缺血性神经元损伤的发病机制包括钙稳态紊乱、兴奋性氨基酸大量释放以及游离氧自由基生成增加。3. 钙拮抗剂可通过电压敏感性钙通道抑制钙离子流入神经元细胞。4. 谷氨酸拮抗剂通过使与NMDA受体相关的钙通道（NMDA拮抗剂）或AMPA/quisqualate受体相连的钠通道（非NMDA拮抗剂）失活来降低细胞内钙离子浓度。5. 此外，氧自由基清除剂可避免神经元损伤。6. 腺苷能和5-羟色胺能递质系统的激动剂通过增加钾离子通透性使神经元膜超极化，从而起到神经保护作用。

Peruche B, Krieglstein J

Institut für Pharmakologie und Toxikologie, Fachbereich Pharmazie und Lebensmittelchemie, Philipps-Universität Marburg, Lahn, Germany.

Prog Neuropsychopharmacol Biol Psychiatry. 1993 Jan;17(1):21-70. doi: 10.1016/0278-5846(93)90032-n.

Oxygen and energy deficits induces a cascade of pathological processes which lead to neuronal dysfunction and cell death. 2. The pathogenesis of ischemia-induced neuronal damage includes a disturbed calcium homeostasis, an excessive release of EAA and an enhanced formation of free oxygen radicals. 3. Calcium antagonists inhibit Ca2+ influx into the neuronal cell via VSCC. 4. Glutamate antagonists reduce intracellular Ca2+ concentration by inactivation of NMDA receptor-associated calcium channels (NMDA antagonists) or AMPA/quisqualate receptor-linked sodium channels (non-NMDA antagonists). 5. Furthermore, oxygen radical scavengers can avoid neuronal damage. 6. Agonists of the adenosinergic and serotonergic transmitter systems contribute to neuroprotection by hyperpolarization of the neuronal membrane due to an increase of K+ permeability.

氧和能量缺乏会引发一系列病理过程，进而导致神经元功能障碍和细胞死亡。2. 缺血性神经元损伤的发病机制包括钙稳态紊乱、兴奋性氨基酸大量释放以及游离氧自由基生成增加。3. 钙拮抗剂可通过电压敏感性钙通道抑制钙离子流入神经元细胞。4. 谷氨酸拮抗剂通过使与NMDA受体相关的钙通道（NMDA拮抗剂）或AMPA/quisqualate受体相连的钠通道（非NMDA拮抗剂）失活来降低细胞内钙离子浓度。5. 此外，氧自由基清除剂可避免神经元损伤。6. 腺苷能和5-羟色胺能递质系统的激动剂通过增加钾离子通透性使神经元膜超极化，从而起到神经保护作用。