Study Finds Vitamin K2 Repairs Nerve Cells By Repairing Mitochondrial Dysfunction
A new function of vitamin K2 has been uncovered — the vitamin inhibits nerve cell damage by repairing mitochondrial dysfunction and reducing oxidative stress.
Vitamin K2 also regulates mitochondrial membrane potential.
The vitamin works by inhibiting nerve cell damage caused by 6-OHDA, a a nerve agent that causes degeneration of dopamine neurons, and regulating apoptosis and autophagy.
In a recent study conducted by a research group led by Prof. ZHENG Zhiming from the Institute of Intelligent Machines, Hefei Institutes of Physical Science (HFIPS), Chinese Academy of Sciences (CAS), scientists found a novel function of vitamin K2 – it can regulate mitochondrial membrane potential and relieve oxidative stress, thereby repairing mitochondrial dysfunction and inhibiting nerve cell damage caused by 6-OHDA.
The related research results were published in Nutrients.
6-Hydroxydopamine (6-OHDA) is a nerve agent that causes degeneration of dopamine neurons, which can lead to mitochondrial damage and nerve cell death. It is often used in the pathogenesis of neurodegenerative disorders.
In this research, scientists found that vitamin K2 can inhibit nerve cell damage caused by 6-OHDA by protecting mitochondria.
Dr.TANG Hengfang, first author of the paper further explained the mechanism as follows: One is to play the role of the master switch of apoptosis by upregulated the expression of Bcl-2 and downregulated the expression of Bax, thereby regulating mitochondrial membrane potential and ROS levels, and alleviating oxidative stress; the other is to maintain the normal operation of mitochondrial fusion, division, autophagy and generation, thereby control the normal operation of the mitochondrial quality control loop and repair damaged mitochondria.
The research results show that vitamin K2 may play a role in the prevention and treatment of neurodegenerative conditions by repairing nerve cell damage.
Vitamin K2 Modulates Mitochondrial Dysfunction Induced by 6-Hydroxydopamine in SH-SY5Y Cells via Mitochondrial Quality-Control Loop