Nicotinamide mononucleotide (NMN) protects bEnd.3 cells against H(2) O(2) -induced damage via NAMPT and the NF-κB p65 signalling pathway

Nicotinamide mononucleotide (NMN) protects bEnd.3 cells against H(2) O(2) -induced damage via NAMPT and the NF-κB p65 signalling pathway

Summary

NMN, or nicotinamide mononucleotide, has been found to have anti-aging, antioxidant, and anti-inflammatory effects. In a study conducted on brain microvascular endothelial cells, it was discovered that NMN inhibits the NF-κBp65 inflammatory signaling pathway and increases the expression of important enzymes. NMN was also found to alleviate oxidative stress and apoptosis in these cells. These findings suggest that NMN has protective effects on cerebrovascular diseases related to diabetes, aging, and oxidative stress.

Blood-brain Barrier Dysfunction and NMN

The blood-brain barrier (BBB) is comprised of specialized endothelial cells that regulate various functions in the brain. Diabetes and other metabolic disorders can lead to dysfunction of these cells and impaired BBB integrity. Oxidative stress and inflammation are key factors in this dysfunction. NMN has been shown to have anti-inflammatory effects, improve endothelial dysfunction, and regulate NAD+ levels in endothelial cells. Its impact on oxidative stress and inflammation in brain endothelial cells and its role in mediating nampt levels are areas that require further exploration.

Experimental Study Findings

In the study mentioned, bEnd.3 cells were used as an in vitro model to investigate the effects of NMN on H2O2-induced oxidative stress and inflammation. Various assays and analyses were performed to assess the viability, apoptosis, mitochondrial membrane potential, reactive oxygen species (ROS) levels, enzyme activity, and gene and protein expression in these cells. The results showed that NMN protected the cells from H2O2-induced decline in proliferation activity, reduced apoptosis, improved mitochondrial function, decreased ROS levels, increased antioxidant enzyme activity, and inhibited the NF-κB p65 inflammatory pathway.

Potential Therapeutic Significance of NMN

This study provides insights into the potential therapeutic significance of NMN in combating oxidative stress, inflammation, and endothelial dysfunction in diabetic cerebral microangiopathy and related conditions. NMN has demonstrated its ability to improve cell vitality, reduce LDH activity, protect against oxidative stress-induced damage, prevent apoptosis, and stabilize endothelial cell function. It achieves these effects by regulating the NF-κB p65 signaling pathway and increasing the expression of NAMPT, eNOs, and VEGF enzymes.

Declaration of Interests and Contributions

The authors of the study declare no conflict of interest. The experimental design was conducted by ZL and XL, with financial support provided by them. XD, CL, and YQ carried out the experiment, while XD wrote the manuscript. All authors contributed to data analysis.

Title of paper: Nicotinamide mononucleotide (NMN) protects bEnd.3 cells against H(2) O(2) -induced damage via NAMPT and the NF-κB p65 signalling pathway

Author(s): Deng X, Liang X, Yang H, Huang Z, Huang X, Liang C, Kuang Y, Qin Y, Lin F, Luo Z.

Year published: 2021

Published in: FEBS Open Bio

Original article can be found here.

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