Dissection on the promising potential of NMN in treating atherosclerosis

Atherosclerosis is a chronic progressive inflammatory disease, which is featured by the accumulation of lipids in the intima of the arteries with yellow appearance. This disease is dominated by coronary artery atherosclerosis and cerebrovascular atherosclerosis, representing the fundamental cause of most cardiovascular diseases, with over 15 million deaths worldwide in 2019.

By virtue of its potent anti-inflammatory and anti-oxidative properties, nicotinamide mononucleotide (NMN), an effective NAD⁺ booster, has promising potential in hampering the progression of atherosclerosis.

The atherosclerotic model is constructed by feeding ApoE−/− mice with high-fat diet (HFD) for 10 weeks until the plaque formation and accumulation in the middle arteries. Subsequently, the model mice are subjected to daily intraperitoneal injection of saline (100 μL) or NMN (500mg/kg) for 8 consecutive weeks (6 days a week). Strikingly, it is found that the weight and food consumption of mice are barely affected post NMN intraperitoneal injection.

NMN greatly dampens the progression of atherosclerosis, as evidenced by the overtly diminished size of atherosclerotic plaque (36 %) and necrotic core (48 %) in aortic sinus, as well as the decreased lipid area (43 %) and increased collagen content (51 %) in atherosclerotic lesions.



Noteworthily, the anti-atherosclerotic effect of NMN may be partially achieved by its anti-oxidative property. In a nutshell, NMN lessens the level of malondialdehyde (MDA), a major biomarker of lipid peroxidation and oxidative stress, yet elevates the levels of anti-oxidant markers superoxide dismutase (SOD) and glutathione peroxidase (GSH-PX) in serum.

NMN regulates macrophages to repress plaque inflammation. There are two main polarization phenotypes for macrophages, where M1 type contributes to pro-inflammatory cytokines production and are deemed to be atherogenic, while the M2 type produces anti-inflammatory cytokines and exerts a preventive effect on the progression of atherosclerosis. NMN promotes the polarization of macrophages to the anti-inflammatory M2 phenotype, as manifested by the downregulation of M1-associated markers (Tnf-α, Il-6, Il-1β and Mcp-1) and upregulation of M2-related markers (Arg-1, Mrc-1, Retlna and Irf-4) in aortic samples.

NMN produces anti-atherosclerotic effects possibly via suppressing oxidative stress and inflammatory response in HFD-fed ApoE−/− mice, hinting its promising potential in the treatment of atherosclerosis.

[1] Vaduganathan M, Mensah GA, Turco JV, et al. The Global Burden of Cardiovascular Diseases and Risk: A Compass for Future Health. J Am Coll Cardiol. 2022;80(25):2361-2371. doi:10.1016/j.jacc.2022.11.005

[2] Wang Z, Zhou SH, Hao YL, et al, Nicotinamide mononucleotide protects against high-fat-diet-induced atherosclerosis in mice and dampens aortic inflammation and oxidative stress. J Functional Foods. 2024 (112): 1756-4646, doi: 10.1016/j.jff.2023.105985.

BONTAC is the pioneer of NMN industry and the first manufacturer to launch NMN mass production, with the first whole-enzyme catalysis technology around the world. At present, BONTAC has become the leading enterprise in niche areas of coenzyme products. Notably, BONTAC is the NMN raw material supplier of famous David Sinclair team at the Harvard University, who uses the raw materials of BONTAC in a paper titled “Impairment of an Endothelial NAD⁺-H₂S Signaling Network Is a Reversible Cause of Vascular Aging”. Our services and products have been highly recognized by global partners. Furthermore, BONTAC has the first national and the only provincial independent coenzyme engineering technology research center in Guangdong, China. The coenzyme products of BONTAC are widely used in fields such as nutritional health, biomedicine, medical beauty, daily chemicals and green agriculture.

This article is based on the reference in the academic journal. The relevant information is provide for sharing and learning purposes only, and does not represent any medical advice purposes. If there is any infringement, please contact the author for deletion. The views expressed in this article do not represent the position of BONTAC.