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阿尔茨海默病样病变对同型半胱氨酸和同型半胱氨酸水平的影响——体内动力学探索性研究。

Effects of Alzheimer-Like Pathology on Homocysteine and Homocysteic Acid Levels-An Exploratory In Vivo Kinetic Study.

机构信息

Fraunhofer Institute for Translational Medicine and Pharmacology ITMP, Theodor-Stern-Kai 7, 60596 Frankfurt am Main, Germany.

Pharmazentrum Frankfurt/ZAFES, Institute of Clinical Pharmacology, Goethe University, Theodor-Stern-Kai 7, 60590 Frankfurt am Main, Germany.

出版信息

Int J Mol Sci. 2021 Jan 18;22(2):927. doi: 10.3390/ijms22020927.

DOI:10.3390/ijms22020927
PMID:33477684
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7831937/
Abstract

Hyperhomocysteinemia has been suggested potentially to contribute to a variety of pathologies, such as Alzheimer's disease (AD). While the impact of hyperhomocysteinemia on AD has been investigated extensively, there are scarce data on the effect of AD on hyperhomocysteinemia. The aim of this in vivo study was to investigate the kinetics of homocysteine (HCys) and homocysteic acid (HCA) and effects of AD-like pathology on the endogenous levels. The mice received a B-vitamin deficient diet for eight weeks, followed by the return to a balanced control diet for another eight weeks. Serum, urine, and brain tissues of knock-in and C57BL/6J wild type mice were analyzed for HCys and HCA using LC-MS/MS methods. Hyperhomocysteinemic levels were found in wild type and knock-in mice due to the consumption of the deficient diet for eight weeks, followed by a rapid normalization of the levels after the return to control chow. Hyperhomocysteinemic mice had significantly higher HCys in all matrices, but not HCA, compared to wild type control. Higher serum concentrations were associated with elevated levels in both the brain and in urine. Our findings confirm a significant impact of AD-like pathology on hyperhomocysteinemia in the mouse model. The immediate normalization of HCys and HCA after the supply of B-vitamins strengthens the idea of a B-vitamin intervention as a potentially preventive treatment option for HCys-related disorders such as AD.

摘要

高同型半胱氨酸血症被认为可能导致多种病理，如阿尔茨海默病（AD）。虽然高同型半胱氨酸血症对 AD 的影响已经得到广泛研究，但关于 AD 对高同型半胱氨酸血症的影响的数据却很少。本体内研究旨在探讨同型半胱氨酸（HCys）和同型半胱氨酸酸（HCA）的动力学以及 AD 样病理对内源性水平的影响。小鼠接受维生素 B 缺乏饮食 8 周，然后再恢复平衡对照饮食 8 周。采用 LC-MS/MS 法分析 knock-in 和 C57BL/6J 野生型小鼠的血清、尿液和脑组织中的 HCys 和 HCA。由于 8 周的缺乏饮食，野生型和 knock-in 小鼠的同型半胱氨酸水平升高，随后在恢复对照饮食后，水平迅速恢复正常。与野生型对照相比，高同型半胱氨酸血症小鼠在所有基质中均具有显著更高的 HCys，但 HCA 则没有。血清浓度升高与大脑和尿液中水平升高有关。我们的研究结果证实了 AD 样病理对 小鼠模型中高同型半胱氨酸血症的显著影响。在供应维生素 B 后，HCys 和 HCA 立即恢复正常，这加强了维生素 B 干预作为 HCys 相关疾病（如 AD）的潜在预防治疗选择的想法。

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