Effect of oxidative stress on disulfide bond formation of uric acid efflux transporter BCRP

氧化应激对尿酸外排转运蛋白BCRP二硫键形成的影响

• 批准号: 22890003
• 负责人: OGURA Jiro
• 金额: $ 2.01万
• 依托单位: Hokkaido University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Research Activity Start-up
• 财政年份: 2010
• 资助国家: 日本
• 起止时间: 2010 至 2011
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-22890003/
• 关键词: 痛風; キサンチンオキシダーゼ; 活性酸素; トランスポータ; ジスルフィド結合

In this study, we investigated that oxidative stress affected BCRP expression, which is a uric acid efflux transporter. It has known that aging-induced oxidative stress is caused by activation of xanthine oxidase. Thus, we used the substrates of xanthine oxidase in this study. In Caco-2 cells, the activation of xanthine oxidase was suppressed the BCRP S-S bond formation, but not in HK-2 cells. These results suggest that the effect of oxidative stress on the efflux of uric acid is different between intestine and kidney.

在这项研究中，我们研究了氧化应激对尿酸外流转运体BCRP表达的影响。已知衰老引起的氧化应激是由黄嘌呤氧化酶的激活引起的。因此，我们在本研究中使用了黄嘌呤氧化酶的底物。在Caco-2细胞中，黄嘌呤氧化酶的激活抑制了BCRP-S-S键的形成，而在HK-2细胞中则没有。这些结果表明，氧化应激对尿酸外流的影响在肠和肾是不同的。

项目成果

(1st/14) Intestinal ischemia-reperfusion increases efflux for uric acid via paracellular route in the intestine, but decreases that via transcellular route mediated by Bcrp

(1st/14) 肠道缺血再灌注会增加肠道中尿酸通过细胞旁途径的流出，但会减少通过 Bcrp 介导的跨细胞途径的尿酸流出

• 发表时间: 2012
• 期刊: J. Pharm. Pharm. Sci
• 作者: Kato N;et al.;藤田恭之;畑中豊,松野吉宏;Ogura J
• 通讯作者: Ogura J