β-Nicotinamide mononucleotide activates NAD+/SIRT1 pathway and attenuates inflammatory and oxidative responses in the hippocampus regions of septic mice

β-Nicotinamide mononucleotide activates NAD+/SIRT1 pathway and attenuates inflammatory and oxidative responses in the hippocampus regions of septic mice

Article Summary: NMN Treatment Shows Promise in Alleviating Memory Dysfunction and Neuroinflammation in Sepsis: A Study on the NAD+/SIRT1 Pathway

Section Headers

  1. Introduction
  2. NMN and the NAD+/SIRT1 Pathway
  3. Study Findings
  4. Implications and Potential Therapeutic Intervention
  5. Study Design and Methods
  6. Conclusion

Introduction

The article discusses the potential of Nicotinamide Mononucleotide (NMN) treatment in alleviating memory dysfunction and neuroinflammation associated with sepsis, specifically in sepsis-associated encephalopathy (SAE). SAE is a common complication characterized by brain dysfunction that lacks effective medication. The NAD+/SIRT1 pathway, which is responsible for cellular aging and metabolism, plays a crucial role in this context.

NMN and the NAD+/SIRT1 Pathway

The study conducted experiments on septic mice and BV-2 cells to investigate the effects of NMN on memory impairment, inflammation, and oxidative stress. Results showed that in septic mice, the activation of the NAD+/SIRT1 pathway in the hippocampus was inhibited, accompanied by increased inflammation. However, NMN treatment restored the NAD+/SIRT1 pathway, improved memory impairment, reduced apoptosis, inflammation, and oxidative stress in the hippocampus.

Study Findings

The protective effects of NMN were reversed by the SIRT1 inhibitor, EX-527, confirming the involvement of the NAD+/SIRT1 pathway. Similar effects were observed in LPS-stimulated BV-2 cells. These findings suggest that NMN treatment may be a potential therapeutic intervention for SAE, as it activates the NAD+/SIRT1 signaling pathway and reduces neuroinflammation and oxidative stress.

Implications and Potential Therapeutic Intervention

It is noted that the study had limitations, such as not investigating the development of sepsis and determining the most suitable NMN dose. The exact mechanism of how NMN regulates SIRT1 expression is also unclear, although DNA methylation may be involved.

Study Design and Methods

In conclusion, NMN treatment shows promising results for alleviating memory dysfunction and neuroinflammation in sepsis. The study highlights the potential therapeutic role of NMN in SAE and underscores the importance of the NAD+/SIRT1 pathway in this context. Further research is needed to explore and optimize the use of NMN as a treatment for sepsis-associated complications.

Conclusion

The article was contributed by researchers Hui-ru Li, Qiang Liu, and Cheng-long Zhu, with the study design and manuscript review conducted by Jia-feng Wang and Xiao-ming Deng. Other researchers assisted in performing the experiments. The authors have disclosed no competing financial interests and declare no personal relationships that could have influenced the study.

Title of paper: β-Nicotinamide mononucleotide activates NAD+/SIRT1 pathway and attenuates inflammatory and oxidative responses in the hippocampus regions of septic mice

Author(s): Li HR, Liu Q, Zhu CL, Sun XY, Sun CY, Yu CM, Li P, Deng XM, Wang JF.

Year published: 2023

Published in: Redox Biol

Original article can be found here.

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