Survey of candidate molecules relevant to diabetic angiopathy

糖尿病血管病相关候选分子的调查

• 批准号: 18500641
• 负责人: FUKATSU Kayoko
• 金额: $ 3.49万
• 依托单位: National Institute of Advanced Industrial Science and Technology
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 2006
• 资助国家: 日本
• 起止时间: 2006 至 2009
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-18500641/
• 关键词: 血管障害; 糖尿病; 酸化ストレス; 培養細胞; グルタチオン; 糖尿病血管障害; 鉄; 血管内皮細胞; 糖化; 生体分子; 生理活性; ストレス; 活性酸素

To investigate the novel candidate molecules involved in the cause of diabetic angiopathy, we used cultured human umbilical vein endothelial cells (HUVEC). In living HUVEC that was exposed to high glucose, antioxidant ability via the GSH cycle was remarkably reduced. The possibility was suggested that glycation of glutathione is responsible for this reduction. Two glycated glutathiones, whose N-position and S-position was respectively modified, were synthesized, and their coenzyme activities for antioxidative enzyme via GSH system were decreased. Further studies in this line would contribute to actual medical treatment in future.

为了研究与糖尿病血管病病因有关的新型候选分子，我们使用了培养的人脐静脉内皮细胞（HUVEC）。在暴露于高葡萄糖的活体 HUVEC 中，谷胱甘肽循环的抗氧化能力显着降低。有人认为谷胱甘肽的糖化可能是造成这种减少的原因。合成了两种N位和S位分别被修饰的糖化谷胱甘肽，其通过GSH系统抗氧化酶的辅酶活性降低。这方面的进一步研究将有助于未来的实际医疗。

项目成果

シスチン・グルタミン酸トランスポーターの発現制御と機能

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• 发表时间: 2007
• 作者: 佐藤英世

Symbiotic bacteria associated with stomach disks of human lice

与人类虱子胃盘相关的共生细菌

• 发表时间: 2006
• 作者: Sasaki

Aggravation of ischemia-reperfusion-triggered acute renal failure in xCT-deficient mice

xCT 缺陷小鼠缺血再灌注引发的急性肾衰竭加重

• 发表时间: 2009
• 作者: Shibasaki; T.; et al. Hideyo Sato (9人中8番目)
• 通讯作者: et al. Hideyo Sato (9人中8番目)

Time-dependent changes in xCT protein expression in the striatum of the hemi-Parkinson rat : use of a new polyclonal antibody

半帕金森大鼠纹状体中 xCT 蛋白表达的时间依赖性变化：使用新型多克隆抗体

• 发表时间: 2008
• 作者: Massie; A.; et al. Hideyo Sato(8人中6番目)
• 通讯作者: et al. Hideyo Sato(8人中6番目)

Expression and function of cystine/glutamate transporter in neutrophils

中性粒细胞中胱氨酸/谷氨酸转运蛋白的表达和功能

• 发表时间: 2007
• 作者: Sakakura; Y.; et al. Hideyo Sato(9人中2番目)
• 通讯作者: et al. Hideyo Sato(9人中2番目)