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设计并合成 6-O-磷酸化肝素硫酸寡糖以抑制淀粉样 β 聚合。

Design and Synthesis of 6-O-Phosphorylated Heparan Sulfate Oligosaccharides to Inhibit Amyloid β Aggregation.

机构信息

Univ. Lille, CNRS, UMR 8576 - UGSF - Unité de Glycobiologie Structurale et Fonctionnelle, 59000, Lille, France.

Department of Biochemistry, Wakayama Medical University, 811-1 Kimiidera, Wakayama, 641-8509, Japan.

出版信息

Chembiochem. 2022 Aug 3;23(15):e202200191. doi: 10.1002/cbic.202200191. Epub 2022 Jun 16.

Abstract

Dysregulation of amyloidogenic proteins and their abnormal processing and deposition in tissues cause systemic and localized amyloidosis. Formation of amyloid β (Aβ) fibrils that deposit as amyloid plaques in Alzheimer's disease (AD) brains is an earliest pathological hallmark. The polysulfated heparan sulfate (HS)/heparin (HP) is one of the non-protein components of Aβ deposits that not only modulates Aβ aggregation, but also acts as a receptor for Aβ fibrils to mediate their cytotoxicity. Interfering with the interaction between HS/HP and Aβ could be a therapeutic strategy to arrest amyloidosis. Here we have synthesized the 6-O-phosphorylated HS/HP oligosaccharides and reported their competitive effects on the inhibition of HP-mediated Aβ fibril formation in vitro using a thioflavin T fluorescence assay and a tapping mode atomic force microscopy.

摘要

淀粉样蛋白的失调及其在组织中的异常加工和沉积会导致全身性和局部性淀粉样变性。淀粉样 β (Aβ) 纤维的形成在阿尔茨海默病 (AD) 大脑中沉积为淀粉样斑块,是最早的病理标志之一。多硫酸化肝素硫酸酯 (HS)/肝素 (HP) 是 Aβ 沉积物中的非蛋白成分之一,不仅调节 Aβ 聚集,而且还作为 Aβ 纤维的受体发挥作用,介导其细胞毒性。干扰 HS/HP 与 Aβ 之间的相互作用可能是阻止淀粉样变性的一种治疗策略。在这里,我们合成了 6-O-磷酸化的 HS/HP 寡糖,并报道了它们在体外使用硫黄素 T 荧光测定法和原子力显微镜( tapping mode atomic force microscopy)测定法抑制 HP 介导的 Aβ 纤维形成方面的竞争作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/54ea/9401075/39dfaebd9605/CBIC-23-0-g005.jpg

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