Jul 24, 2023 / Author: China Glutathione suppliers & NMN manufacturers
In recent years, the phenomenon of an increasingly aging global population has aroused great interest in aging-related research, especially in the search for rejuvenating molecules that may delay aging and enhance regeneration of the aging central nervous system (CNS). To this end, the team of Professor Zhao Jingwei from Zhejiang University School of Medicine, Jinan University and Fudan University jointly published a research paper entitled "Reintroducing Sirtuin 2 into the nucleus of oligodendrocyte precursor cells helps promote remyelination during aging".
Through various research methods, the research team found that supplementing NMN, the immediate precursor of NAD+, can promote the expression and nuclear entry of SIRT2 in aged OPCs, thereby enhancing the differentiation of aged OPCs, delaying myelin aging, and promoting the repair of myelin sheath damage.
In experiments in rats, the gene expression of oligodendrocyte precursor OPCs was significantly increased after supplementation with NAD+ precursor NMN, and the mRNA levels of most genes involved in metabolism were also significantly downregulated.
At the same time, NMN supplementation can also promote the proliferation and differentiation of aging OPCs, thereby delaying the aging of myelin in the normal central nervous system and enhancing the myelin repair of the central nervous system.
Based on these findings, NMN supplementation could increase NAD+ levels, restore the nuclear entry of SIRT2 in OPCs, and deacetylate H3K18, thereby inhibiting the transcription of ID4 and further promoting OPC differentiation.
Restoration of NAD+ promotes the differentiation of OPCs into mature oligodendrocytes, ultimately delaying myelin aging and enhancing repair capacity in the central nervous system. This study provides new ideas and hope for finding treatments that may delay aging and enhance CNS regeneration.
This paper shows that supplementation of β-NMN can increase the expression and nuclear import of SIRT2 in aged OPCs, thereby promoting the differentiation of aged OPCs, delaying myelin aging and promoting the repair of myelin after injury.
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