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机译:促红细胞生成素对氯胺酮诱导的大鼠皮质神经元凋亡的保护作用:PI3K / Akt和GSK-3 beta途径的参与
Department of Anesthesiology Union Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan 430022 China;
Department of Neurology Union Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan China;
Department of Anesthesiology Union Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan 430022 China;
Tongji Medical College Huazhong University of Science and Technology Wuhan China;
Department of Anesthesiology Union Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan 430022 China;
Department of Neurology Dongfeng Hospital Shiyan China;
Erythropoietin; Ketamine; Cortical neurons; Neuroprotection; Akt; GSK-3β; Caspase-3;
机译:促红细胞生成素对氯胺酮诱导的大鼠皮质神经元凋亡的保护作用:PI3K / Akt和GSK-3 beta途径的参与
机译:埃德拉龙酮通过减少氧化应激和激活PI3K / AKT信号途径来保护从氯胺酮诱导的细胞凋亡的培养培养的大鼠皮质神经元。
机译:17β-雌二醇通过激活PI3K / Akt / Bcl-2信号传导,保护原代培养的大鼠皮质神经元免受氯胺酮诱导的细胞凋亡。
机译:PI3K / AKT /GSK3β途径参与神经元和胶质细胞的光动力损伤
机译:多靶点受体酪氨酸激酶抑制剂利尼法尼(ABT-869)通过磷酸肌醇3激酶(PI3K)/ AKT依赖性信号传导途径诱导凋亡并抑制白血病细胞的增殖。
机译:米诺环素对氯胺酮诱导的神经干细胞损伤的保护作用:PI3K / Akt和Gsk-3 Beta途径的参与。
机译:米诺环素对氯胺酮致神经干细胞损伤的保护作用:参与pI3K / akt和Gsk-3β途径