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Research and Development of Neuroprotective Drugs Based on the Neuron-Glia Interactions

Research and Development of Neuroprotective Drugs Based on the Neuron-Glia Interactions
基于神经元-胶质细胞相互作用的神经保护药物的研发
批准号:
11557004
负责人:
BABA Akemichi
金额:
$8.64万
依托单位:
依托单位国家:
日本
项目类别:
Grant-in-Aid for Scientific Research (B)
财政年份:
1999
资助国家:
日本
项目状态:
已结题
起止时间:
1999 至 2001

项目摘要

项目成果

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相关文献

中文摘要
翻译
新药的神经保护作用;钠/钙交换抑制剂SEA400减少大脑中动脉闭塞所致的脑梗塞体积(J。实验298,249-256,2001)。SEA400对热损伤所致脑损伤的脑水肿(含水量增加)也有抑制作用。抗水肿作用部分来自血脑屏障的保护作用。T-588是一种用于治疗阿尔茨海默病的新药,它通过激活细胞外调节蛋白激酶(ERK)来预防氧化应激对培养星形胶质细胞的损伤。药剂399,1-8,2000)。注射T-588可增加大鼠脑内ERK活性。一项免疫化学研究表明,T-588对ERK激活的增加是由于神经元成分所致。这些发现提示SEA400和T-588可能是脑损伤和神经退行性疾病的神经保护药物。胶质细胞死亡的机制;血清剥夺诱导培养的小胶质细胞死亡是由促凋亡蛋白Bax的表达介导的。乔拉莫尔。83,351-154,2000)。对培养的星形胶质细胞的凋亡机制进行研究。我们发现,诱导星形胶质细胞的凋亡与线粒体膜电位的降低密切相关。几种药物(T-588、异丁司特、CV-2619.SEA400)可预防。《星形细胞凋亡》杂志,133,841-578,2001;实验298,249-256,2001)。CGMP介导的细胞内信号参与了线粒体膜电位的调节,从而保护星形胶质细胞的凋亡。
英文摘要
Neuroprotective Actions of Novel Drugs; SEA400, a Na/Ca exchange inhibitor decreased the brain infract volume induced by MCA occlusion (Jpharmacol. Exp. Ther., 298,249-256,2001). SEA400 also had an inhibitory effect on brain edema (increases in water content) in heat lesion-induced brain injury. The anti-edema effect was partly brought from protection of BBB. T-588, a novel drug aimed for therapy of Alzheimer disease, prevented damages of cultured astrocytes by oxidartive stress, which was mediated by the activation of ERK (extracellular-regulated protein kinase) (Eur. Jpharmacol 399,1-8,2000). Injection of T-588 increased ERK activity in rat brain. An immunochemical study, showed that the increase in ERK activation by T-588 is due to the neuronal component. These findings suggest a possibility that SEA400 and T-588 could be neuroprotective drugs against brain injury and neurodegenerative diseases.Mechanisms of Glial Death; Serum-deprivation-induced death of cultured microglia was mediated by expression: of Bax, an pro-apoptotic protein (Jpn. Jpharmacol. 83,351-154,2000). Mechanisms of apoptosis of cultured astrocytes were examined. We found that induction of astrocytes apoptosis was closely related with reduction of mitochondrial membrane potential. Several drugs (T-588, Ibudilast, CV-2619.SEA400) prevented. The astrocytic apoptosis Br.Jpharmacol., 133,841-578, 2001; Jpharmacol. Exp. Ther., 298,249-256,2001). Intracelluair signals mediated by cGMP were involved in the regulation mitochondrial membrane potential to protect astrocytic apoptosis.
期刊论文(200)
专著(0)
科研奖励(0)
会议论文
Baba A.: "Glial activation and death"Saishinn-lgaku. 54. 75-78 (1999)
Baba A.:“神经胶质的激活和死亡”Saishinn-lgaku。
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通讯作者:
Koyama Y.: "Endothelin In brain"Nou-21. 4. 73-78 (2001)
小山 Y.:“脑内皮素”Nou-21。
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通讯作者:
Koyama Y.: "focal adhesion kinase and paxillin accompanied with their Endothelins increase tyrosine phosphorylation of astrocytic association with cytoskeletal components"Neuroscience. 101. 219-227 (2000)
Koyama Y.:“粘着斑激酶和桩蛋白及其内皮素增加了与细胞骨架成分相关的星形胶质细胞的酪氨酸磷酸化”神经科学。
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通讯作者:
Hitoshi Hashimoto: "Genomic organization and chromosomal location of the mouse vasoactive intestinal polypeptide 1 (VPACl) receptor"Genomics. 58. 90-93 (1999)
Hitoshi Hashimoto:“小鼠血管活性肠多肽1(VPAC1)受体的基因组组织和染色体位置”基因组学。
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