Suppr超能文献

甘油醛导致SH-SY5Y人神经母细胞瘤细胞中诊断标志物水平出现阿尔茨海默病样改变。

Glyceraldehyde caused Alzheimer's disease-like alterations in diagnostic marker levels in SH-SY5Y human neuroblastoma cells.

作者信息

Koriyama Yoshiki, Furukawa Ayako, Muramatsu Michiru, Takino Jun-ichi, Takeuchi Masayoshi

机构信息

Graduate School and Faculty of Pharmaceutical Sciences, Suzuka University of Medical Science, Suzuka, Mie, 513-8670, Japan.

Department of Pathophysiological Science, Faculty of Pharmaceutical Science, Hokuriku University, Kanazawa, Ishikawa, 920-1181, Japan.

出版信息

Sci Rep. 2015 Aug 25;5:13313. doi: 10.1038/srep13313.

Abstract

Clinical evidence has implicated diabetes mellitus as one of the risk factors for the development and progression of Alzheimer's disease (AD). However, the neurotoxic pathway activated due to abnormalities in glucose metabolism has not yet been identified in AD. In order to investigate the relationship between impaired cerebral glucose metabolism and the pathophysiology of AD, SH-SY5Y human neuroblastoma cells were exposed to glyceraldehyde (GA), an inhibitor of glycolysis. GA induced the production of GA-derived advanced glycation end-products (GA-AGEs) and cell apoptosis, glycolytic inhibition, decreases in the medium concentrations of diagnostic markers of AD, such as amyloid β 1-42 (Aβ42), and increases in tau phosphorylation. These results suggest that the production of GA-AGEs and/or inhibition of glycolysis induce AD-like alterations, and this model may be useful for examining the pathophysiology of AD.

摘要

临床证据表明,糖尿病是阿尔茨海默病(AD)发生和进展的危险因素之一。然而,AD中尚未确定因葡萄糖代谢异常而激活的神经毒性途径。为了研究脑葡萄糖代谢受损与AD病理生理学之间的关系,将SH-SY5Y人神经母细胞瘤细胞暴露于糖酵解抑制剂甘油醛(GA)中。GA诱导了GA衍生的晚期糖基化终产物(GA-AGEs)的产生和细胞凋亡、糖酵解抑制、AD诊断标志物(如淀粉样β 1-42(Aβ42))的培养基浓度降低以及tau磷酸化增加。这些结果表明,GA-AGEs的产生和/或糖酵解抑制会诱导AD样改变,该模型可能有助于研究AD的病理生理学。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1249/4548441/6607b9eacb79/srep13313-f1.jpg

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验