Augmented O-GlcNAc signaling via glucosamine attenuates oxidative stress and apoptosis following contrast-induced acute kidney injury in rats

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• 作者：Jiachang Hu^a ; ^b ; ^c ; ^d ; ¹ ; Rongyi Chen^a ; ^b ; ^c ; ^d ; ¹ ; Ping Jia^a ; ^b ; ^c ; ^d ; Yi Fang^a ; ^b ; ^c ; ^d ; Tongqiang Liu^e ; Nana Song^a ; ^b ; ^c ; ^d ; Xialian Xu^a ; ^b ; ^c ; ^d ; Jun Ji^a ; ^b ; ^c ; ^d ; ^{ji.jun@zs-hospital.sh.cn} ; Xiaoqiang Ding^a ; ^b ; ^c ; ^d ; ^{ding.xiaoqiang@zs-hospital.sh.cn}
• 关键词：Acute kidney injury ; Iodinated contrast media ; Hexosamine biosynthetic pathway ; Glycogen synthase kinase-3β
• 刊名：Free Radical Biology and Medicine
• 出版年：2017
• 出版时间：February 2017
• 年：2017
• 卷：103
• 期：Complete
• 页码：121-132
• 全文大小：2632 K
• 卷排序：103

文摘

Increasing evidence suggests that O-linked β-N-acetylglucosamine (O-GlcNAc) levels are increased in response to stress and that acute augmentation of this reaction is cytoprotective. We used a novel and reliable contrast-induced acute kidney injury (CI-AKI) model and the results showed that augmented O-GlcNAc signaling by glucosamine prevented the kidneys against iohexol-induced injury by the attenuation of apoptosis and oxidative stress. Furthermore, both alloxan and specific inhibitors of PI3K (Wortmannin and LY294002) blocked the protection of glucosamine via inhibiting Akt signaling pathway.