Recently, a research team from China Agricultural University has made a breakthrough in the field of cardiovascular disease research
NMN reduces the size of atherosclerotic plaques (36%) and necrotic cores (48%) in the aortic sinus. NMN reduced lipid area in atherosclerotic lesions (43%) and increased collagen content (51%).
NMN decreases serum malondialdehyde (MDA) levels and increases the enzymatic activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-PX). NMN decreases the expression of pro-inflammatory factors (TNF, IL-1, IL-6, and MCP-1) and increases the expression of anti-inflammatory factors (ARG-1, MRC-1, RETLNA, and IRF-4) in aortic tissue.
It is understood that this study is the world's first experiment to test NMN on an animal model of atherosclerosis. In the experiment, the researchers reproduced the formation and accumulation of plaque in the middle arteries in humans by feeding mice a diet high in cholesterol and fat. Mice are injected with NMN (at a dose of 500 mg kg) daily for 8 consecutive weeks (6 days per week).
It was found that there was no significant difference in blood lipids between the mice in the saline group and the NMN group, except for weight and food consumption. This indicated that NMN did not affect the body weight or appetite of mice, which laid a foundation for further exploration of the specific mechanism and effect of NMN on atherosclerosis in subsequent experiments.
Figure 1A protocol for the intervention of NMN in atherosclerosis in mice.
Two major effects:
NMN can inhibit atherosclerosis
In the process of analyzing the size and lipid profile of atherosclerotic plaques, the researchers found that: compared to a control group injected with saline alone, the researchersNote**NMN mice had a 36% reduction in atherosclerotic plaque areaThis suggests that NMN helps to reduce plaque formation. In addition,NMN also reduced lipid deposition in atherosclerotic lesions, making it 43% lower.
Further histological analysis also found that compared to the saline group,The proportion of late lesions decreased by 25% in mice with NMN**, while the proportion of early lesions increased by 42%. This means that NMN may have helped stop the further progression of atherosclerosis.
Summarizing the above results, it can be concluded that:NMN may help reduce atherosclerotic plaque load and lipid deposition in mice.
Figure 2NMN inhibits the formation of atherosclerotic lesions in mice.
NMN prevents arterial plaque from rupturing
In the process of studying the stability of NMN on atherosclerotic plaques, the researchers found:Compared to the control group injected with saline only, the necrotic core of mice injected with **NMN was significantly smaller, with a 48% reduction. In addition, NMN treatment makes atherosclerotic plaquesCollagen content increased by 51%.This further supports the conclusion that NMN contributes to plaque stability. These results show that:NMN helps to improve the stability of atherosclerotic plaques in mice, preventing arterial plaque rupture.
Figure 3NMN inhibits arteriosclerotic necrotic core formation and reduces collagen content in mice.
Two main ways to protect:
NMN antioxidant prevents atherosclerosis
In the process of studying whether NMN can reduce oxidative stress in mice, the researchers found:NMN treatment significantly reduced MDA (a marker of lipid peroxidation and oxidative stress) levels in mouse serumThis means that lipid peroxidation is reduced. At the same time,Levels of SOD and GSH-PX (two enzymes that help the body fight oxidative stress) also increasedThis indicates that the antioxidant capacity of mice has been improved. These results suggest that NMN may inhibit the progression of atherosclerosis through its antioxidant capacity.
Figure 4NMN enhances antioxidant capacity in mice.
NMN regulates macrophage anti-plaque inflammation
In the study of whether NMN inhibits the inflammatory response of plaques by regulating the polarization of macrophages, the researchers found that NMN inhibited the gene expression of M1 macrophages (which can produce pro-inflammatory cytokines), and at the same time, NMN enhanced the gene expression of M2 macrophages (which can produce anti-inflammatory cytokines). This means that NMN is able to promote the transformation of macrophages into a more anti-inflammatory M2 phenotype, thereby inhibiting the inflammatory response in plaques. 
Figure 5Effect of NMN on the expression of pro-inflammatory and anti-inflammatory genes in mouse aortic samples.
Overall, research from China Agricultural University revealed that NMN can not only effectively inhibit atherosclerosis, but also help improve the stability of atherosclerotic plaques in mice and prevent arterial plaque rupture. And inhibition of atherosclerosis through antioxidant mechanisms, as well as inhibition of plaque inflammation response by regulating macrophage polarization, providing a new strategy for the prevention and inhibition of atherosclerosis.
About atherosclerosis
Atherosclerosis is a common vascular disease characterized by the accumulation of fat and calcium in the lining of the arteries, causing the walls of the blood vessels to thicken, stiffen, and lose their elasticity, which in turn leads to narrowing of the lumen of the blood vessels. This disease mainly affects the large and middle arteries, such as coronary arteries, carotid arteries, cerebral arteries, renal arteries, etc., and can lead to a variety of cardiovascular diseases, such as coronary heart disease, cerebral infarction, peripheral vascular disease, etc.
The pathogenesis of atherosclerosis is not fully understood, but studies have found that the disease is related to a variety of factors, such as dyslipidemia, hypertension, diabetes, smoking, obesity, etc. These factors may lead to pathological processes such as endothelial cell damage, inflammatory response, and oxidative stress, which in turn lead to the occurrence and progression of atherosclerosis.
References: Zi Wang, Shuaishuai Zhou, Yanling Hao, Tiancheng Xu, Peng An, Yongting Luo, Junjie Luo, Nicotinamide mononucleotide protects against high-fat-diet-induced atherosclerosis in mice and Dampens Aortic Inflammation and Oxidative Stress,Journal of Functional Foods,Volume 112,2024,105985,ISSN 1756-4646,The content of this article is from academic journals, and the relevant information is for sharing and learning only, and does not represent any medical advice. If there is any infringement, please write to the author of this article to delete, and the views in this article do not represent the position of Bangtai Biotech.