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在大脑缺血/再输血损伤期间,揭示影响维生素B₁₂的 lysosomal malondialdehyde

Di Su¹, Ran Zhang¹, Xin Wang¹

¹College of Chemistry, Chemical Engineering and Materials Science, Collaborative Innovation Center of Functionalized Probes for Chemical Imaging in Universities of Shandong, Key Laboratory of Molecular and Nano Probes, Ministry of Education, Institutes of Biomedical Sciences, Shandong Normal University, Jinan 250014, Shandong, People's Republic of China.

Journal of the American Chemical Society

|October 7, 2023

概括

在脑缺血重灌损伤 (CIRI) 中,溶解体甲酸 (MDA) 阻断了维生素B12的运输. 这一MDA-LMBD1轴解释了CIRI中的维生素B12治疗失败,并提供了一个新的治疗点.

科学领域:

神经科学
生物化学
细胞生物学

背景情况:

大脑缺血-再输损伤 (CIRI) 涉及同素 (Hcy) 的上调,导致神经毒性.
维生素B12补充剂通常用于降低Hcy,但对CIRI无效.
lysosomal 氧化应激,以 malondialdehyde (MDA) 表示,可能会阻碍维生素 B12 的运输.

研究的目的:

调查溶酶MDA是否会干扰CIRI中的维生素B12运输.
开发一种实时,现场测量活脑中的 lysosomal MDA 的方法.
在CIRI期间阐明维生素B12治疗无效的机制.

主要方法:

光成像剂Lyso-MCBH的构建,用于 lysosomal MDA 的检测.
使用Lyso-MCBH的CIRI在小鼠体内监测溶酶体MDA水平.
评估溶解体MDA对维生素B12运输和LMBD1功能的影响.

主要成果:

在CIRI期间,Lyso- MCBH成功监测了活小鼠大脑中的溶酶体MDA.
观察到升高的溶酶体MDA阻碍了从溶酶体到细胞质的维生素B12输送.
过度的溶酶体MDA对维生素B12载体LMBD1的表达和功能产生了负面影响.

结论:

溶解体MDA通过影响LMBD1来阻碍维生素B12的运输,这解释了CIRI中的治疗失败.
解体MDA-LMBD1轴被确定为CIRI发病的一个关键因素.
在CIRI中准这一轴是提高维生素B12功效的潜在治疗策略.

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