Pharmacology and Potential Implications of Nicotinamide Adenine Dinucleotide Precursors

She, Jing; Sheng, Rui; Qin, Zheng‐Hong

doi:10.14336/ad.2021.0523

Cited by 23 publications

(20 citation statements)

References 186 publications

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“…Nicotinamide is the precursor of coenzyme-I and coenzyme-II. Coenzyme-I and coenzyme-II are coenzymes of dehydrogenase and transfer material in the body for lipid metabolism and glycolysis [20,21]. In the present study, the level of nicotinamide in the liver samples of normal rats was increased after the administration of ascending medicine, indicating that ascending medicine can promote energy metabolism in the liver by enhancing the production of nicotinamide, while the nicotinamide level was decreased in the descending TCM group.…”

Section: Effects Of Ascending and Descending Medicine On Liversupporting

confidence: 48%

Systemic metabolomics characterization of the ascending and descending property

Liu

Zhou

et al. 2023

Preprint

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Background According to the theory of TCM, ascending medicine has the effects of elevating yang, raising drooping, and inducing sweating. Descending medicine has the effects of relieving dyspnea and hiccup, stopping reflux, and calming nerves. In conclusion, the ascending/descending properties of TCM serve as a guide for the use of TCMs in clinical practice. However, at present, there are few studies on the ascending/descending properties of TCM. This study aimed to compare the effects of 6 ascending and 8 descending medicine on the main organs (heart, liver, lung, spleen, and kidney) of normal rats, characterizing the ascending and descending properties. Methods The orgain samples of all experiment group were analyzed based on ultra performance liquid chromatography-quadrupole time of flight mass spectrometry (UPLC-Q/TOFMS). Then, to character the ascending and descending properties, the effects of 6 ascending and 8 descending medicine on the main organs (heart, liver, lung, spleen, and kidney) of normal rats were compared. Results The systemic metabolomics results indicated that linoleic acid metabolism and arginine and proline metabolism were the major differential pathways affected by ascending/descending medicine in the heart; nicotinic acid and nicotinamide metabolism, glutamic acid and glutathione metabolism, and L-carnitine metabolism were the major differential pathways affected by ascending/descending medicine in the liver; tryptophan metabolism, phenylalanine metabolism, and pyroglutamic acid and glutamic acid metabolism were the major differential pathways affected by ascending/descending medicine in the lung; tryptophan metabolism, phenylalanine metabolism, and glutamic acid metabolism were the major differential pathways affected by ascending/descending medicine in the kidney; and glutamic acid and glutamine metabolism were the major differential pathway affected by ascending/descending medicine in the spleen. Conclusions Ascending medicine exhibited positive effects on nerve stimulation, immunity, and reproductive function by promoting energy metabolism in the heart and liver, whereas descending medicine had the opposite effect. Descending medicine exhibited a positive effect on diuresis by promoting blood circulation, whereas ascending medicine had the opposite effect. Both descending medicine and ascending medicine intervened with pulmonary inflammation, but the underlying mechanisms may be different. This study demonstrated that systemic metabolomics technology can be used for the characterization of traditional Chinese medicine properties.

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Section: Effects Of Ascending and Descending Medicine On Liversupporting

confidence: 48%

Systemic metabolomics characterization of the ascending and descending property

Liu

Zhou

et al. 2023

Preprint

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“…NAM is also known to inhibit PARP-1, a NAD consuming enzyme that is activated by reperfusion injury [6]. On the other hand, the direct absorption of NAD + by cells is limited due to its large polarity [11]. In this study, we found that supplementation with NAM rapidly restored cardiac tissue NAD + content, enhanced glycolysis and ATP generation while reducing glucose shunting to sorbitol, promoted recovery of contractile function and improved mouse survival after cardiac arrest.…”

Section: Introductionmentioning

confidence: 53%

Nicotinamide restores tissue NAD+ and improves survival in rodent models of cardiac arrest

Zhu,

Li,

Wang

et al. 2023

PLoS ONE

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Metabolic suppression in the ischemic heart is characterized by reduced levels of NAD+ and ATP. Since NAD+ is required for most metabolic processes that generate ATP, we hypothesized that nicotinamide restores ischemic tissue NAD+ and improves cardiac function in cardiomyocytes and isolated hearts, and enhances survival in a mouse model of cardiac arrest. Mouse cardiomyocytes were exposed to 30 min simulated ischemia and 90 min reperfusion. NAD+ content dropped 40% by the end of ischemia compared to pre-ischemia. Treatment with 100 μM nicotinamide (NAM) at the start of reperfusion completely restored the cellular level of NAD+ at 15 min of reperfusion. This rescue of NAD+ depletion was associated with improved contractile recovery as early as 10 min post-reperfusion. In a mouse model of cardiac arrest, 100 mg/kg NAM administered IV immediately after cardiopulmonary resuscitation resulted in 100% survival at 4 h as compared to 50% in the saline group. In an isolated rat heart model, the effect of NAM on cardiac function was measured for 20 min following 18 min global ischemia. Rate pressure product was reduced by 26% in the control group following arrest. Cardiac contractile function was completely recovered with NAM treatment given at the start of reperfusion. NAM restored tissue NAD+ and enhanced production of lactate and ATP, while reducing glucose diversion to sorbitol in the heart. We conclude that NAM can rapidly restore cardiac NAD+ following ischemia and enhance glycolysis and contractile recovery, with improved survival in a mouse model of cardiac arrest.

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“…NMN is one of the natural compounds to boost NAD + biosynthesis. In mammals, NMN can be produced from nicotinamide (NAM, a form of vitamin B3 found in various foods) by nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme [ 21 , 27 , 28 ]. NMN can also be synthesized from nicotinamide riboside (NR) through NR kinase-mediated phosphorylation reaction.…”

Section: Discussionmentioning

confidence: 99%

“…In this regard, NMN supplementation could increase NAD + biosynthesis. In fact, numerous experimental studies showed its relationship under their experimental conditions in not only the central nervous system but also other types of body systems [ 21 , 27 , 28 ]. Chen et al showed that retinal NAD + levels increased by NMN treatment in the retinal detachment-induced damaged retina [ 11 ].…”

Section: Discussionmentioning

confidence: 99%

Nicotinamide Mononucleotide Protects against Retinal Dysfunction in a Murine Model of Carotid Artery Occlusion

Lee

Tomita

Miwa

et al. 2022

IJMS

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Cardiovascular abnormality-mediated retinal ischemia causes severe visual impairment. Retinal ischemia is involved in enormous pathological processes including oxidative stress, reactive gliosis, and retinal functional deficits. Thus, maintaining retinal function by modulating those pathological processes may prevent or protect against vision loss. Over the decades, nicotinamide mononucleotide (NMN), a crucial nicotinamide adenine dinucleotide (NAD+) intermediate, has been nominated as a promising therapeutic target in retinal diseases. Nonetheless, a protective effect of NMN has not been examined in cardiovascular diseases-induced retinal ischemia. In our study, we aimed to investigate its promising effect of NMN in the ischemic retina of a murine model of carotid artery occlusion. After surgical unilateral common carotid artery occlusion (UCCAO) in adult male C57BL/6 mice, NMN (500 mg/kg/day) was intraperitoneally injected to mice every day until the end of experiments. Electroretinography and biomolecular assays were utilized to measure ocular functional and further molecular alterations in the retina. We found that UCCAO-induced retinal dysfunction was suppressed, pathological gliosis was reduced, retinal NAD+ levels were preserved, and the expression of an antioxidant molecule (nuclear factor erythroid-2-related factor 2; Nrf2) was upregulated by consecutive administration of NMN. Our present outcomes first suggest a promising NMN therapy for the suppression of cardiovascular diseases-mediated retinal ischemic dysfunction.

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Pharmacology and Potential Implications of Nicotinamide Adenine Dinucleotide Precursors

Cited by 23 publications

References 186 publications

Systemic metabolomics characterization of the ascending and descending property

Systemic metabolomics characterization of the ascending and descending property

Nicotinamide restores tissue NAD+ and improves survival in rodent models of cardiac arrest

Nicotinamide Mononucleotide Protects against Retinal Dysfunction in a Murine Model of Carotid Artery Occlusion

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