磷酸吡哆醛通过HS/AKT/GSK3β信号轴减轻大鼠心脏与年龄相关的代谢失衡。
Pyridoxal-5-phosphate mitigates age-related metabolic imbalances in the rat heart through the HS/AKT/GSK3β signaling axis.
作者信息
Strutynska Nataliia A, Balatskyi Volodymyr V, B Strutynskyi Ruslan, Goshovska Yulia V, Mys Lidiia A, Luchkova Alina Yu, Denysova Maiia V, Korkach Yuliia P, Strutynskyi Vladyslav R, Piven Oksana O, Dobrzyn Pawel, Sagach Vadym F
机构信息
The Department of Blood Circulation of Bogomoletz Institute of Physiology of the National Academy of Sciences of Ukraine, Kyiv, Ukraine. Address: 4, Bogomoletz Str., Kyiv 01024, Ukraine.
The Laboratory of Molecular Medical Biochemistry of Nencki Institute of Experimental Biology, Polish Academy of Sciences. Address: 3 Pasteur Str., Warsaw 02-093, Poland.
出版信息
Mitochondrion. 2025 Mar;81:102001. doi: 10.1016/j.mito.2024.102001. Epub 2025 Jan 2.
Pyridoxal-5-phosphate (PLP) enhances the synthesis of endogenous hydrogen sulfide, a potent regulator of cell metabolism. We used 24-month-old rats to investigate the PLP mitoprotective function in the aging heart. We demonstrated improvement of mitochondrial bioenergetic functions, inhibition of mPTP opening after PLP administration. Moreover, PLP treatment increased glucose consumption and utilization, decreased lipid transport into the cells, but increased fatty acid β-oxidation, providing sufficient energy. An ECG study showed a significant improvement in cardiac function in PLP-treated old rats. Our data suggest that PLP may exert its effect through the HS/AKT/GSK3β axis with further targeting of the Sirt1/PGC-1α signaling pathway.
磷酸吡哆醛（PLP）可增强内源性硫化氢的合成，硫化氢是细胞代谢的一种有效调节剂。我们使用24月龄大鼠来研究PLP在衰老心脏中的线粒体保护功能。我们证明了给予PLP后线粒体生物能量功能得到改善，线粒体通透性转换孔（mPTP）开放受到抑制。此外，PLP处理增加了葡萄糖的消耗和利用，减少了脂质向细胞内的转运，但增加了脂肪酸β-氧化，从而提供了足够的能量。一项心电图研究表明，PLP处理的老年大鼠心脏功能有显著改善。我们的数据表明，PLP可能通过HS/AKT/GSK3β轴发挥作用，并进一步靶向Sirt1/PGC-1α信号通路。
Zotero 插件