Nicotinamide mononucleotide protects against high-fat-diet-induced atherosclerosis in mice and dampens aortic inflammation and oxidative stress

Abstract

Atherosclerosis, a chronic inflammatory disease, is the major cause of arteriosclerotic cardiovascular diseases. Nicotinamide mononucleotide (NMN), an effective NAD+ booster, has been shown to reduce inflammation and protect vascular cell function, which are strongly associated with the progression of atherosclerosis. In this study, we explored the anti-atherosclerotic effects of NMN and its potential mechanism in ApoE−/− mice. We found that NMN significantly reduced the size of atherosclerotic plaque (36 %) and necrotic core (48 %) in aortic sinus. Additionally, NMN decreased lipid area (43 %) and increased collagen content (51 %) in atherosclerotic lesions. In addition, NMN reduced the level of malondialdehyde (MDA) in serum while elevating the enzymatic activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-PX). Moreover, NMN reduced the expression of pro-inflammatory cytokines (Tnfα, Il-1β, Il-6 and Mcp-1) while increased the expression of anti-inflammatory factors (Arg-1, Mrc-1, Retlna and Irf-4) in aortic tissues. These results indicate that NMN exerts anti-atherosclerotic effects and inhibits oxidative stress and inflammatory response in HFD-fed ApoE−/− mice.

Keywords

• Atherosclerosis
• Nicotinamide mononucleotide
• Anti-oxidant
• Anti-inflammatory