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Blockade of the Formation of Insoluble Ubiquitinated Protein Aggregates by EGCG3Me in the Alloxan-Induced Diabetic Kidney

机译:EGCG3 Me抑制四氧嘧啶诱导的糖尿病肾中不溶性泛素化蛋白质聚集体的形成

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摘要

BackgroundRenal accumulation of reactive carbonyl compounds (RCCs) has been linked to the progression of diabetic nephropathy. We previously demonstrated that carbonyl stress induces the formation of amino-carbonyl cross-links and sharply increases the content of β-sheet-rich structures, which is the seed of insoluble aggregates formation, and tea catechin (-)-epigallocatechin 3-gallate (EGCG) can reverse this process in vitro and in vivo. In this study, methylated derivative (-)-epigallocatechin-3-O-(3-O-methyl)-gallate (EGCG3”Me) was hypothesized to neutralize carbonyl stress mediating the formation of insoluble ubiquitinated protein (IUP) aggregates, and reduce the early development of diabetic nephropathy.
机译:背景活性羰基化合物(RCCs)的肾脏积累与糖尿病性肾病的进展有关。先前我们证明了羰基应力会诱导氨基-羰基交联的形成并急剧增加富含β-折叠的结构的含量,这是不溶性聚集物形成的种子,而茶儿茶素(-)-表没食子儿茶素3-没食子酸酯( EGCG)可以在体外和体内逆转这一过程。在这项研究中,假设甲基化衍生物(-)-表没食子儿茶素3-O-(3-O-甲基)-没食子酸酯(EGCG3” Me)可中和羰基应激,介导不溶性泛素化蛋白(IUP)聚集体的形成,并减少糖尿病肾病的早期发展。

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