Noninvasive assessment of the brain redox status in chronic kidney disease mouse using overhauser-enhanced magnetic resonance imaging

使用奥豪瑟增强磁共振成像对慢性肾病小鼠的脑氧化还原状态进行无创评估

• 批准号: 20790039
• 负责人: YAMATO Mayumi
• 金额: $ 2.75万
• 依托单位: Kyushu University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Young Scientists (B)
• 财政年份: 2008
• 资助国家: 日本
• 起止时间: 2008 至 2009
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-20790039/
• 关键词: イメージング; グルタミン酸; 脳; 腎不全; レドックス

Urea toxin is suggested to be induced the glutamatergic neuronal damage mediated by the activity of N-methyl-D-aspartate (NMDA) receptor. In this study, we aimed to demonstrate brain redox alterations in chronic kidney disease mouse noninvasively, using overhauser-enhanced magnetic resonance imaging (OMRI).The reduction rate of 3-methoxycarbonyl-2,2,5,5-tetramethylpyrrolidine-l-oxyl (methoxycarbonyl-PROXYL), a redox-sensitive contrast agent, was used as an index of the redox status in vivo. No changes were seen in the 8-OHdG (8-Hydroxydeoxyguanosine) or the memory disturbance at 2 or 4 weeks after CKD onset, but after 4 weeks of CKD, the methoxycarbonyl-PROXYL reduction rate, calculated from continuous images, had increased significantly. At 8 weeks after CKD onset, we observed an increase in the number of 8-OHdG-immunopositive cells and the disturbance in the memory. Thus, the noninvasive imaging of the brain redox alterations was associated with the initial stages of CKD cause brain injury.

建议尿素毒素被诱导由N-甲基-D-天冬氨酸（NMDA）受体的活性介导的谷氨酸能神经元损伤。 In this study, we aimed to demonstrate brain redox alterations in chronic kidney disease mouse noninvasively, using overhauser-enhanced magnetic resonance imaging (OMRI).The reduction rate of 3-methoxycarbonyl-2,2,5,5-tetramethylpyrrolidine-l-oxyl (methoxycarbonyl-PROXYL), a redox-sensitive contrast agent, was used as an index of体内氧化还原状态。在CKD发作后2或4周的8-OHDG（8-羟基氧基鸟苷）或记忆障碍中未见变化，但是在CKD 4周后，甲氧基碳酸苯甲酰 - 羟基降低速度，从连续图像中计算出来的甲氧基碳酸苯基降低速率已显着增加。在CKD发作后的第8周内，我们观察到8-OHDG免疫阳性细胞的数量和记忆中的干扰增加。因此，脑氧化还原改变的无创成像与CKD的初始阶段有关导致脑损伤。