Mechanism of ischemic tolerance phenomenon in hippocampal CAI sector of the gerbil
沙鼠海马CAI区缺血耐受现象的机制
基本信息
- 批准号:05671185
- 负责人:
- 金额:$ 1.34万
- 依托单位:
- 依托单位国家:日本
- 项目类别:Grant-in-Aid for General Scientific Research (C)
- 财政年份:1993
- 资助国家:日本
- 起止时间:1993 至 1995
- 项目状态:已结题
- 来源:
- 关键词:
项目摘要
Following brief cerebral ischemia, tolerance to subsequent ischemia is induced in the hippocampal neurons. The aim of this study was to investigate the relationship between ischemic tolerance phenomenon and protein synthesis. First, recovery of protein synthesis was studied autoradiographically in gerbils with induced tolerance. To observe the effect of tolerance acquisition, double forebrain ischemia, 2-min ischemia followed by 5 min-ischemia, was induced 2 days later. In this group, recovery of protein synthesis in the CAI sector was rapid. At 1 day of recirculation, protein synthesis returned near normal. On the other hand, protein synthesis in the 5-min ischemia group was severely suppressed and never returned to the normal level. The present study revealed an early recovery of protein synthesis in the hippocampal neurons in the gerbil with induced tolerance. Secondly, possible differences in electrophoresis pattern of the brain protein between tolerance-induce animals and animals injected with protein synthesis inhibitor. There was no differences in the pattern of the protein between these two groups. Thirdly, we investigated whether multiple sublethal ishemia can enhance the ability of tolerance induction or prolong the period of tolerance. At 1 month after the multiple exposure to sublethal 2-min ischemia, animals did not acquire ischemic tolerance to 4-min lethal ischemia. To clarify the mechanism of ischemic tolerance, further studies are needed.
短暂的脑缺血后,海马神经元对随后的缺血产生耐受。本研究旨在探讨缺血耐受现象与蛋白质合成的关系。首先,恢复蛋白质的合成进行了研究放射自显影在沙鼠诱导耐受。为观察耐受获得的效果,在2天后诱导双前脑缺血,缺血2min,再缺血5min。在该组中,CAI区蛋白质合成的恢复很快。在再循环的第1天,蛋白质合成恢复接近正常。另一方面,5分钟缺血组的蛋白质合成受到严重抑制,从未恢复到正常水平。本研究揭示了早期恢复的蛋白质合成在海马神经元中诱导耐受的沙鼠。第二,耐受诱导动物和蛋白质合成抑制剂注射动物脑蛋白质电泳图谱的可能差异。这两组之间的蛋白质模式没有差异。第三,探讨了多次亚致死性缺血是否能增强耐受诱导能力或延长耐受时间。在多次暴露于亚致死性2分钟缺血后1个月,动物没有获得对4分钟致死性缺血的缺血耐受。缺血耐受的机制有待进一步研究。
项目成果
期刊论文数量(20)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
Nakagomi T,Kirino T,Kanemitsu H,Tsujita Y,Tamura A: "Early recovery of protein synthesis following ischemia in tolerance-induced hippocampal neurons in the gerbil." J Cereb Blood Flow Metab. 13. S581 (1993)
Nakagomi T、Kirino T、Kanemitsu H、Tsujita Y、Tamura A:“沙鼠耐受诱导的海马神经元缺血后蛋白质合成的早期恢复。”
- DOI:
- 发表时间:
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- 影响因子:0
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- 通讯作者:
Nakagomi T,Asai A,Kanemitsu H,Narita K,Kuchino Y,Tamura A,Kirino T: "Up-regulation of c-myc gene expression following focal ischemia in the rat brain." Neurol Res. (in press).
Nakagomi T、Asai A、Kanemitsu H、Narita K、Kuchino Y、Tamura A、Kirino T:“大鼠脑局灶性缺血后 c-myc 基因表达上调。”
- DOI:
- 发表时间:
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- 影响因子:0
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- 通讯作者:
Nakagomi T, et al:"Up-regulation of c-myc gene expression following focal ischemia in the rat brain" J. Cereb Blood Flow and Metabol. 15. S407 (1995)
Nakagomi T 等人:“大鼠脑局部缺血后 c-myc 基因表达的上调”J. Cereb 血流和代谢。
- DOI:
- 发表时间:
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- 影响因子:0
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中込忠好,浅井昭雄,田村晃,他: "Ischemia Grand Round CVD Grand Round Series vol 2" に-ろん社(桐野高明編), 174 (1995)
中込忠义、浅井昭夫、田村彰等:《Ischemia Grand Round CVD Grand Round Series vol 2》Ni-ronsha(桐野高明编辑),174(1995)
- DOI:
- 发表时间:
- 期刊:
- 影响因子:0
- 作者:
- 通讯作者:
Nakagomi T.,Tamura A.: "Eary recovery of protein synthesis following ischemia in hippocampal neurons with induced tolerance in the gerbil." Acta Neuropathol. 86. 10-15 (1993)
Nakagomi T.,Tamura A.:“海马神经元缺血后蛋白质合成的早期恢复,并诱导沙鼠的耐受性。”
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- 影响因子:0
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NAKAGOMI Tadayoshi其他文献
NAKAGOMI Tadayoshi的其他文献
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{{ truncateString('NAKAGOMI Tadayoshi', 18)}}的其他基金
Basic studies for prevention and treatment of the ischemic neuronal death
缺血性神经元死亡防治的基础研究
- 批准号:
08457374 - 财政年份:1996
- 资助金额:
$ 1.34万 - 项目类别:
Grant-in-Aid for Scientific Research (B)
The role of arachidonic acid cascade in the development of delayed neuronal death
花生四烯酸级联在迟发性神经元死亡发展中的作用
- 批准号:
01570802 - 财政年份:1989
- 资助金额:
$ 1.34万 - 项目类别:
Grant-in-Aid for General Scientific Research (C)
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