2021年8月31日
Validation of the mitochondrial delivery of vitamin B1 to enhance ATP production using SH-SY5Y cells, a model neuroblast.
Journal of pharmaceutical sciences
- ,
- ,
- ,
- 巻
- 111
- 号
- 2
- 開始ページ
- 432
- 終了ページ
- 439
- 記述言語
- 英語
- 掲載種別
- 研究論文(学術雑誌)
- DOI
- 10.1016/j.xphs.2021.08.033
Large amounts of ATP are produced in mitochondria especially in the brain and heart, where energy consumption is high compared with other organs. Thus, a decrease in ATP production in such organs could be a cause of many diseases such as neurodegenerative diseases and heart disease. Based on thus assumption, increasing intracellular ATP production in such organs could be a therapeutic strategy. In this study, we report on the delivery of vitamin B1, a coenzyme that activates the tricarboxylic acid (TCA) cycle, to the inside of mitochondria. Since the TCA cycle is responsible for ATP production, we hypothesized delivering vitamin B1 to mitochondria would enhance ATP production. To accomplish this, we used a mitochondrial targeted liposome a "MITO-Porter" as the carrier. Using SH-SY5Y cells, a model neuroblast, cellular uptake and intracellular localization were analyzed using flow cytometry and confocal laser scanning microscopy. The optimized MITO-Porter containing encapsulated vitamin B1 (MITO-Porter (VB1)) was efficiently accumulated in mitochondria of SH-SY5Y cells. Further studies confirmed that the level of ATP production after the MITO-Porter (VB1) treatment was significantly increased as compared to a control group that was treated with naked vitamin B1. This study provides the potential for an innovative therapeutic strategy in which the TCA cycle is activated, thus enhancing ATP production. Relative ATP ratio (%) = IS/IU × 100, where IS and IU represent the intracellular ATP amounts for the treated and untreated cells with samples, respectively.
- リンク情報
- ID情報
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- DOI : 10.1016/j.xphs.2021.08.033
- PubMed ID : 34478755