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维生素 B12 可减轻 SH-SY5Y 细胞中与氧化应激相关的磷脂水平变化。

Vitamin B12 Attenuates Changes in Phospholipid Levels Related to Oxidative Stress in SH-SY5Y Cells.

机构信息

Experimental Neurology, Saarland University, 66424 Homburg, Germany.

Nutrition Therapy and Counseling, Campus Gera, SRH University of Applied Health Science, 07548 Gera, Germany.

出版信息

Cells. 2022 Aug 18;11(16):2574. doi: 10.3390/cells11162574.

DOI:10.3390/cells11162574
PMID:36010649
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9406929/
Abstract

Oxidative stress is closely linked to Alzheimer's disease (AD), and is detected peripherally as well as in AD-vulnerable brain regions. Oxidative stress results from an imbalance between the generation and degradation of reactive oxidative species (ROS), leading to the oxidation of proteins, nucleic acids, and lipids. Extensive lipid changes have been found in post mortem AD brain tissue; these changes include the levels of total phospholipids, sphingomyelin, and ceramide, as well as plasmalogens, which are highly susceptible to oxidation because of their vinyl ether bond at the sn-1 position of the glycerol-backbone. Several lines of evidence indicate that a deficiency in the neurotropic vitamin B12 is linked with AD. In the present study, treatment of the neuroblastoma cell line SH-SY5Y with vitamin B12 resulted in elevated levels of phosphatidylcholine, phosphatidylethanolamine, sphingomyelin, and plasmalogens. Vitamin B12 also protected plasmalogens from hydrogen peroxide (HO)-induced oxidative stress due to an elevated expression of the ROS-degrading enzymes superoxide-dismutase (SOD) and catalase (CAT). Furthermore, vitamin B12 elevates plasmalogen synthesis by increasing the expression of alkylglycerone phosphate synthase (AGPS) and choline phosphotransferase 1 (CHPT1) in SH-SY5Y cells exposed to HO-induced oxidative stress.

摘要

氧化应激与阿尔茨海默病(AD)密切相关,可在外周和 AD 易损脑区检测到。氧化应激是由于活性氧(ROS)的产生和降解之间失衡引起的,导致蛋白质、核酸和脂质氧化。在 AD 脑组织的死后组织中发现了广泛的脂质变化;这些变化包括总磷脂、神经鞘磷脂和神经酰胺以及血浆类脂的水平,由于其甘油骨架 sn-1 位置的乙烯醚键,这些物质极易氧化。有几条证据表明,神经营养维生素 B12 的缺乏与 AD 有关。在本研究中,用维生素 B12 处理神经母细胞瘤细胞系 SH-SY5Y,导致磷脂酰胆碱、磷脂酰乙醇胺、神经鞘磷脂和血浆类脂的水平升高。维生素 B12 还通过提高 ROS 降解酶超氧化物歧化酶(SOD)和过氧化氢酶(CAT)的表达,保护血浆类脂免受过氧化氢(HO)诱导的氧化应激。此外,维生素 B12 通过增加 HO 诱导的氧化应激下 SH-SY5Y 细胞中烷基甘油磷酸合酶(AGPS)和胆碱磷酸转移酶 1(CHPT1)的表达,增加血浆类脂的合成。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0c19/9406929/4fde392971ed/cells-11-02574-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0c19/9406929/acd08aa1a521/cells-11-02574-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0c19/9406929/11a58c2f5b0a/cells-11-02574-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0c19/9406929/469117f70cb9/cells-11-02574-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0c19/9406929/25c9869309da/cells-11-02574-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0c19/9406929/4fde392971ed/cells-11-02574-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0c19/9406929/acd08aa1a521/cells-11-02574-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0c19/9406929/af8e48f9aa47/cells-11-02574-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0c19/9406929/11a58c2f5b0a/cells-11-02574-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0c19/9406929/469117f70cb9/cells-11-02574-g004.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0c19/9406929/4fde392971ed/cells-11-02574-g006.jpg

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