The ischemic tolerance induced by electromagnetic field exposure.

电磁场暴露引起的缺血耐受。

基本信息

批准号：
13671625
负责人：
HARADA Hideki
金额：
$ 2.24万
依托单位：
Kurume University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2001
资助国家：
日本
起止时间：
2001 至 2003
项目状态：
已结题

项目摘要

Introduction : It has been suggested that magnetic field promotes the Heat Shock Protein 70 gene expression and synthesis, could cause a rapid induction of the immediate-early genes known to play one of the major roles in acquisition of ischemic preconditioning in the central nervous system. In this study we have tested in rats the hypothesis that electromagnetic field (EMF) could make neurons more tolerant to subsequent lethal forebrain ischemia. Materials and Methods : Wistar rats were randomly allocated to one of six experimental groups. Sham animals with restraint stress and EM field exposure were subjected to sham operation. Non-stimulated (Control) and stimulated groups with 8 Hz, 25 Hz and 50 Hz of EMF (2mT) were subjected to lethal forebrain ischemia at 2 days after pretreatment. The brain ischemia was achieved by 4-vessel occlusion technique and was applied for 5 or 8 mm. Seven days after the ischemic insults, the injury of CA1 neurons was examined in coronal planes 3.3-mm posterior to the bregma. Through light microscopic examination, viable and nonviable neurons were counted manually in a double-blinded fashion. Results : The CA1 sector was not damaged at all by pretreatment with EME and restraint stress. The Control pretreated with restraint stress followed by 5 and 8 mm of ischemia produced moderate to severe reduction in the CA1 pyramidal cells depending on the length of ischemia respectively. The pretreatment with EMF followed by 8 mm of ischemia did not protect the CA1 pyramidal cell. By contrast, CA1 pyramidal cells were preserved against 5 mm of ischemia in animals pretreated with EMF of 25 Hz but not preserved with EMF of 8 and 50 Hz. Conclusion: The data suggest that EMF at 2 days before ischemia have a possibility to reduce potential effect on the reduction of subsequent mild ischemic brain damage.

简介：有人提出，磁场促进热休克蛋白 70 基因的表达和合成，可能导致立即早期基因的快速诱导，这些基因在中枢神经系统缺血预处理的获得中发挥主要作用之一。在这项研究中，我们在大鼠身上测试了电磁场（EMF）可以使神经元对随后的致命前脑缺血更耐受的假设。材料和方法：Wistar 大鼠被随机分配到六个实验组之一。对具有束缚应激和电磁场暴露的假动物进行假手术。未刺激（对照）和刺激组（8 Hz、25 Hz 和 50 Hz EMF (2mT)）在预处理后 2 天进行致死性前脑缺血。通过4血管闭塞技术实现脑缺血，并应用5或8毫米。缺血性损伤后 7 天，在前囟后 3.3 毫米的冠状面上检查 CA1 神经元的损伤。通过光学显微镜检查，以双盲方式对存活和非存活神经元进行手动计数。结果：通过 EME 和约束应力预处理，CA1 扇区完全没有受到损伤。用约束应力预处理的对照物随后进行5毫米和8毫米的缺血，分别根据缺血的长度产生中度至重度的CA1锥体细胞减少。 EMF 预处理后进行 8 mm 缺血并不能保护 CA1 锥体细胞。相比之下，在用 25 Hz 的 EMF 预处理的动物中，CA1 锥体细胞可以抵抗 5 mm 的缺血，但在 8 和 50 Hz 的 EMF 下则不能保存。结论：数据表明，缺血前 2 天的 EMF 有可能减少随后的轻度缺血性脑损伤的潜在效果。