Nicotinamide mononucleotide and melatonin counteract myocardial ischemia-reperfusion injury by activating SIRT3/FOXO1 and reducing apoptosis in aged male rats

Jafari-Azad, Aida; Hosseini, Leila; Rajabi, Mojgan; Høilund‐Carlsen, Poul Flemming; Vafaee, Manouchehr Seyedi; Feyzizadeh, Saeid; Badalzadeh, Reza

doi:10.1007/s11033-021-06351-8

Cited by 14 publications

(3 citation statements)

References 27 publications

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“…NMN supplementation reduced adiposity in mice, and it had stronger effects on liver fat catabolism and synthesis even in comparison to exercise [45]. The NMN-mediated increase of NAD + levels has been shown to protect the heart from ischemia/reperfusion injury, sustains the neural stem/progenitor cell population, reestablishes skeletal muscle mitochondrial function and arterial function in aged mice, and facilitates mitochondrial function [46,47]. These results indicate that NMN can be quickly absorbed, efficiently transported in blood circulation, and taken up and converted to NAD + in different tissues.…”

Section: Discussionmentioning

confidence: 99%

Oral Administration of Nicotinamide Mononucleotide Increases Nicotinamide Adenine Dinucleotide Level in an Animal Brain

et al. 2022

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As a redox-sensitive coenzyme, nicotinamide adenine dinucleotide (NAD+) plays a central role in cellular energy metabolism and homeostasis. Low NAD+ levels are linked to multiple disease states, including age-related diseases, such as metabolic and neurodegenerative diseases. Consequently, restoring/increasing NAD+ levels in vivo has emerged as an important intervention targeting age-related neurodegenerative diseases. One of the widely studied approaches to increase NAD+ levels in vivo is accomplished by using NAD+ precursors, such as nicotinamide mononucleotide (NMN). Oral administration of NMN has been shown to successfully increase NAD+ levels in a variety of tissues; however, it remains unclear whether NMN can cross the blood–brain barrier to increase brain NAD+ levels. This study evaluated the effects of oral NMN administration on NAD+ levels in C57/B6J mice brain tissues. Our results demonstrate that oral gavage of 400 mg/kg NMN successfully increases brain NAD+ levels in mice after 45 min. These findings provide evidence that NMN may be used as an intervention to increase NAD+ levels in the brain.

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Section: Discussionmentioning

confidence: 99%

Oral Administration of Nicotinamide Mononucleotide Increases Nicotinamide Adenine Dinucleotide Level in an Animal Brain

et al. 2022

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“…In addition, melatonin upregulated the Bcl-2, sirtuin 3, and FOXO type 1 gene expression, as well as downregulated the Bax and caspase-3 gene expression. Therefore, melatonin may protect the aged heart against ischemia/reperfusion injury by inhibiting apoptosis and activating the sirtuin 3/FOXO1 signaling pathway (Jafari-Azad et al, 2021). A similar study also showed cardio protective effects of melatonin against ischemia/reperfusion injury in aged hearts because it lowered oxidative stress, enhanced mitochondrial membrane potential, and restored the NAD + /NADH ratio (Hosseini et al, 2020).…”

Section: Melatonin As a Therapeutic Agent Useful In The Treatment Of ...mentioning

confidence: 78%

Melatonin as an Anti-Aging Therapy for Age-Related Cardiovascular and Neurodegenerative Diseases

Giménez

Heras

Lahera

et al. 2022

Front. Aging Neurosci.

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The concept of “aging” is defined as the set of gradual and progressive changes in an organism that leads to an increased risk of weakness, disease, and death. This process may occur at the cellular and organ level, as well as in the entire organism of any living being. During aging, there is a decrease in biological functions and in the ability to adapt to metabolic stress. General effects of aging include mitochondrial, cellular, and organic dysfunction, immune impairment or inflammaging, oxidative stress, cognitive and cardiovascular alterations, among others. Therefore, one of the main harmful consequences of aging is the development and progression of multiple diseases related to these processes, especially at the cardiovascular and central nervous system levels. Both cardiovascular and neurodegenerative pathologies are highly disabling and, in many cases, lethal. In this context, melatonin, an endogenous compound naturally synthesized not only by the pineal gland but also by many cell types, may have a key role in the modulation of multiple mechanisms associated with aging. Additionally, this indoleamine is also a therapeutic agent, which may be administered exogenously with a high degree of safety. For this reason, melatonin could become an attractive and low-cost alternative for slowing the processes of aging and its associated diseases, including cardiovascular and neurodegenerative disorders.

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“…8 b). NAM is essential for cardiovascular health through enhancing myocardial homeostasis and inhibiting cardiomyocyte apoptosis 27 . Excessive exercise is attributed to myocardial ischemia and hypoxia, leading to significantly decreased NAM and exercise-induced fatigue in rats 28 , 29 .…”

Section: Discussionmentioning

confidence: 99%

Effect of acute high-intensity exercise on myocardium metabolic profiles in rat and human study via metabolomics approach

Wang

Cao

et al. 2022

Sci Rep

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Acute high-intensity exercise can affect cardiac health by altering substance metabolism. However, few metabolomics-based studies provide data on the effect of exercise along with myocardial metabolism. Our study aimed to identify metabolic signatures in rat myocardium during acute high-intensity exercise and evaluate their diagnostic potential for sports injuries. We collected rat myocardium samples and subjects’ serum samples before and after acute high-intensity exercise for metabolite profiling to explore metabolic alterations of exercise response in the myocardium. Multivariate analysis revealed myocardium metabolism differed before and after acute high-intensity exercise. Furthermore, 6 target metabolic pathways and 12 potential metabolic markers for acute high-intensity exercise were identified. Our findings provided an insight that myocardium metabolism during acute high-intensity exercise had distinct disorders in complex lipids and fatty acids. Moreover, an increase of purine degradation products, as well as signs of impaired glucose metabolism, were observed. Besides, amino acids were enhanced with a certain protective effect on the myocardium. In this study, we discovered how acute high-intensity exercise affected myocardial metabolism and exercise-related heart injury risks, which can provide references for pre-competition screening, risk prevention, and disease prognosis in competitive sports and effective formulation of exercise prescriptions for different people.

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Nicotinamide mononucleotide and melatonin counteract myocardial ischemia-reperfusion injury by activating SIRT3/FOXO1 and reducing apoptosis in aged male rats

Cited by 14 publications

References 27 publications

Oral Administration of Nicotinamide Mononucleotide Increases Nicotinamide Adenine Dinucleotide Level in an Animal Brain

Oral Administration of Nicotinamide Mononucleotide Increases Nicotinamide Adenine Dinucleotide Level in an Animal Brain

Melatonin as an Anti-Aging Therapy for Age-Related Cardiovascular and Neurodegenerative Diseases

Effect of acute high-intensity exercise on myocardium metabolic profiles in rat and human study via metabolomics approach

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