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Visualization of calcium signals in acute thromboembolic model of stroke

中风急性血栓栓塞模型中钙信号的可视化

基本信息

批准号：
09470294
负责人：
KANAMARU Kenji
金额：
$ 6.78万
依托单位：
Mie University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (B)
财政年份：
1997
资助国家：
日本
起止时间：
1997 至 1999
项目状态：
已结题

项目摘要

The increase in intracellular calcium ion plays a pivotal in processing vital function. Both necrosis and apoptosis are triggered by the influx of calcium ion via plasma membrane. The stimuli, such as ischemia and trauma, enhance permeability of calcium ion through plasma membrane. The elevation of intracellular calcium ion activates various proteolytic enzymes and caspases. If the calcium ion level reaches high enough to cause cell dysfunction, either apoptosis or necrosis may be programmed. One can surmise that cell death may be prevented by the inhibition of calcium overload. However, distribution of calcium signals during cerebral ischemia has not yet been demonstrated. We developed a novel method to detect calcium signals in the rat cerebral cortex after thromboembolic ischemia. Exposed rat cerebral cortex was preloaded with fra-2 AM, then Rose Bengal was injected intravenously. The proximal middle cerebral artery was irradiated producing thrombosis with 540 nm wavelength green light. Thereafter, ischemic cerebral cortex was alternatively irradiated with 340 and 380 nm light to emit chemiluminescence. The intensity of chemiluminescence took a peak at 60 minutes after the alternative irradiation. The highest calcium signals occurred in ischemic core which was proved by the pathological examination. In ischemic penumbra calcium signal was moderate. No calcium signal was demonstrated in normal cortex. The region of ischemic penumbra deemed a therapeutic target of rescue from cell death. In conclusion, we demonstrated for the first time calcium signals in the ischemic cerebral cortex in vivo.

细胞内钙离子的增加在生命功能的处理中起着关键作用。细胞坏死和细胞凋亡都是由钙离子通过质膜内流引起的。缺血、创伤等刺激可使钙离子透过质膜的能力增强。细胞内钙离子的升高激活各种蛋白水解酶和半胱天冬酶。如果钙离子水平高到足以引起细胞功能障碍，则可以编程凋亡或坏死。可以推测，细胞死亡可以通过抑制钙超载来防止。然而，脑缺血时钙信号的分布尚未得到证实。我们开发了一种新的方法来检测大鼠大脑皮层血栓栓塞性缺血后的钙信号。暴露的大鼠大脑皮层预先装载fra-2 AM，然后静脉注射虎红。用540 nm波长的绿色光照射近端大脑中动脉，产生血栓。此后，缺血的大脑皮质交替地用340和380 nm光照射以发射化学发光。化学发光强度在交替照射后60分钟出现峰值。病理检查证实缺血中心钙信号最强。缺血半暗带钙信号中等。在正常皮质中没有钙信号。缺血半暗带区域被认为是从细胞死亡中拯救的治疗靶点。总之，我们第一次证明了钙信号在体内缺血大脑皮层。