Ischemic Neuronal Damade and heat Shock (Stress) Protein
缺血性神经元损伤和热休克(应激)蛋白
基本信息
- 批准号:02670635
- 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:1990
- 资助国家:日本
- 起止时间:1990 至 1991
- 项目状态:已结题
- 来源:
- 关键词:
项目摘要
We investigated the possibility that neuronal cells given a hyperthermic or mild ischemia treatment acquired tolerance to a subsequent, and what would be lethal, ischemic stress in vivo.Hyperthermia was produced in the rat by placing them in a water bath maintained at 42゚ C. The body temperature of the rat was raised to 42゚ C for 15 min and then the animals were subjected to 15 min of four-vessel occlusion. Seven days after recirculation, the animals were sacrificed, and the brains were removed, fixed in 10% formalin and stained by hematoxylin-eosin for histopathology. In the rat subjected to 15 min of four-vessel occlusion 8 or 24 hours after hyperthermia, ischemic neuronal change in the CA1 was less compared to 15 min of four-vessel occlusion without hyperthermia. The hippocampus from animals subjected to hyperthermia was analysed using immunoblotting. Expression of heat shock proteon 70(HSP 70)was shown in the animals 8 or 24 hours after hyperthermia.Eight min ischemia 24 hours before 15 min ischemia exhibited protective effect against ischemic neuronal change. Expression of HSP 70 was shown in the hippocampus 24 hours after 8 min ischemia, but was not after 15 min ischemia.These results provides support for the possibility that hyperthermia or mild ischemia makes the neuronal cells more resistant to the ischemic damage. It is suggested that these tolerance to the ischemic stress correlates to expression of HSP 70.
我们研究了神经元细胞接受高温或轻度缺血处理后,对随后的、致命的体内缺血应激获得耐受的可能性。将大鼠的体温升高至42 ° C持续15分钟,然后使动物经受15分钟的四血管闭塞。再循环后7天,处死动物,取出脑,固定在10%福尔马林中,并通过苏木精-伊红染色进行组织病理学检查。在高温后8或24小时进行15分钟的四血管闭塞的大鼠中,与没有高温的四血管闭塞15分钟相比,CA 1的缺血性神经元变化较少。使用免疫印迹法分析来自经受高温的动物的海马体。热休克蛋白70(HSP 70)在热疗后8h和24 h均有表达,缺血24 h后再缺血8 min对缺血性神经元损伤有保护作用。缺血8 min后24 h海马可见HSP 70的表达,而缺血15 min后海马未见HSP 70的表达,提示高温或轻度缺血可增强神经细胞对缺血损伤的抵抗能力。提示这种对缺血应激的耐受与HSP 70的表达有关.
项目成果
期刊论文数量(2)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
H.Mabe,A.Umemura H.Kanai,H.Nagai: "The effect of hyper thermia on ischemic neuronal demage" Journal of Cerebral Blood Flow and Metabolism. 11. S121 (1991)
H.Mabe,A.Umemura H.Kanai,H.Nagai:“热疗对缺血性神经元损伤的影响”脑血流和代谢杂志。
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- 影响因子:0
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- 通讯作者:
H.Mabe,A.Umemura,H.kamai,and H.Nagai: "The effect of hyperthermia on ischemic neuronal damage" Journal of Cerebrl Blood Flow and Mefabolism. 11. (1991)
H.Mabe、A.Umemura、H.kamai 和 H.Nagai:“热疗对缺血性神经元损伤的影响”《脑血流和新陈代谢》杂志。
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- 影响因子:0
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MABE Hideo其他文献
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{{ truncateString('MABE Hideo', 18)}}的其他基金
Role of protein kinase C in thedevelopment of ischemic brain edema
蛋白激酶C在缺血性脑水肿发生中的作用
- 批准号:
04670868 - 财政年份:1992
- 资助金额:
$ 1.34万 - 项目类别:
Grant-in-Aid for General Scientific Research (C)
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