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Advantages of NMNH
NMNH: 1. “Bonzyme” Whole-enzymatic method, environmental-friendly, no harmful solvent residues manufacturing powder. 2. Bontac is a very first manufacture in the world to produce the NMNH powder on the level of high purity, stability. 3. Exclusive “Bonpure” seven-step purification technology, high purity（up to 99%) and stability of production of NMNH powder 4. Self-owned factories and obtained a number of international certifications to ensure high quality and stable supply of products of NMNH powder 5. Provide one-stop product solution customization service
Advantages of NADH
NADH: 1. Bonzyme whole-enzymatic method, environmental-friendly, no harmful solvent residues 2. Exclusive Bonpure seven-step purification technology, purity up higher than 98 % 3. Special patented process crystal form, higher stability 4. Obtained a number of international certifications to ensure high quality 5. 8 domestic and foreign NADH patents, leading the industry 6. Provide one-stop product solution customization service
Advantages of NAD
NAD: 1. “Bonzyme” Whole-enzymatic method, environmental-friendly, no harmful solvent residues 2. Stable supplier of 1000+ enterprises around the world 3. Unique “Bonpure” seven-step purification technology, higher product content and higher conversion rate 4. Freeze drying technology to ensure stable product quality 5. Unique crystal technology, higher product solubility 6. Self-owned factories and obtained a number of international certifications to ensure high quality and stable supply of products
Advantages of MNM
NMN: 1. “Bonzyme”Whole-enzymatic method, environmental-friendly, no harmful solvent residues 2. Exclusive“Bonpure”seven-step purification technology, high purity（up to 99.9%) and stability 3. Industrial leading technology: 15 domestic and international NMN patents 4. Self-owned factories and obtained a number of international certifications to ensure high quality and stable supply of products 5. Multiple in vivo studies show that Bontac NMN is safe and effective 6. Provide one-stop product solution customization service 7. NMN raw material supplier of famous David Sinclair team of Harvard University
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Bontac Bio-Engineering (Shenzhen) Co., Ltd. (hereafter referred to as BONTAC) is a high-tech enterprise established in July 2012. BONTAC integrates R&D, production and sales, with enzyme catalysis technology as the core and coenzyme and natural products as main products. There are six major series of products in BONTAC, involving coenzymes, natural products, sugar substitutes, cosmetics, dietary supplements and medical intermediates.
As the leader of the global NMN industry, BONTAC has the first whole-enzyme catalysis technology in China. Our coenzyme products are widely used in health industry, medical & beauty, green agriculture, biomedicine and other fields. BONTAC adheres to independent innovation, with more than 170 invention patents. Different from the traditional chemical synthesis and fermentation industry, BONTAC has advantages of green low-carbon and high-value-added biosynthesis technology. What’s more, BONTAC has established the first coenzyme engineering technology research center at the provincial level in China which also is the sole in Guangdong Province.
In the future, BONTAC will focus on its advantages of green, low-carbon and high-value-added biosynthesis technology, and build ecological relationship with academia as well as upstream/downstream partners, continuously leading the synthetic biological industry and creating a better life for human beings.
NADH manufacturer | NADH and NAD+ are a pair of redox pairs in cells, NADH is the reduced form of coenzyme 1NAD, and NAD+ is its oxidized form. In redox reactions, NADH acts as a donor of hydrogen and electrons, and NAD+ acts as an acceptor of hydrogen and electrons, participating in physiological processes such as respiration, photosynthesis, and alcohol metabolism. They participate in life activities as coenzymes of many oxidation-reduction reactions in organisms and transform each other. Under anaerobic conditions, glucose metabolism produces very little ATP, while under aerobic conditions, NADH or FADH2 produced through glycolysis and tricarboxylic acid cycle can produce a large amount of ATP through oxidative phosphoric acid reaction. The amount of NADH is directly related to the amount of ATP produced, the more NADH each cell contains, the more energy it produces. Organs that require more energy will contain (or require) higher amounts of NADH.
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The Importance of NAD Metabolism in White Adipose Tissue
1. Introduction Nicotinamide adenine dinucleotide (NAD) compartmentalized in adipocytes can modulate adipocyte differentiation and gene expression, in addition to controlling glucose metabolism. White adipose tissue (WAT), one major adipose tissue, may be one of the direct target for NAD supplementation. 2. About WAT In contrast to brown adipose tissue (BAT), WAT contains a single lipid droplet and few mitochondria. WAT, once thought to be morphologically and functionally unremarkable, is in fact highly dynamic, with plasticity and heterogeneity, which is widely distributed in the subcutaneous tissues and around the internal organs. WAT plays a key role in a range of biological processes, such as maintenance of energetic homeostasis, processing and handling of glycans and lipids, blood pressure control, and host defence, with tight relationship with metabolic disorders such as diabetes. 3. The tissue-specific roles of NAD NMN is synthesized from NAM and NR by NAMPT and NRK, respectively. The synthesized NAD+ from NMN is used as a SIRT1 substrate, which leads to the recycling of NAD+ via the salvage pathway. In this process, NAD+ can exert different effects depending on the tissue. Remarkably, NAD precursors can control metabolic stress particularly via focusing on adipose tissue. 4. The effects of boosting NAD+ on WAT Supplementation of NMN and NR has been shown to reduce body weight and enhance insulin sensitivity in regular chow-fed aged wild-type mice and diet-induced obese mice, respectively. NAM supplementation diminishes fat accumulation in diet-induced obese mice. Additionally, both NMN and NR supplementation prevent inflammation even with different treatment duration. NAM administration boosts mitochondrial biogenesis and glutathione synthesis in WAT. Similarly, it is evidenced that NMN treatment in high fat diet-induced type 2 diabetes mouse model facilitates the recovery of Glutathione S-transferase Alpha 2 (Gsta2) gene expression in the liver. 5. The adipose-specific effects of nicotinamide phosphoribosyltransferase (NAMPT) NAMPT, one NAD regulator in WAT, is a promising therapeutic target for the treatment of metabolic disorders. NAMPT plays a potential role in maintaining adipose tissue homoeostasis, as evidenced by the explicitly blocked adipocyte differentiation and lipid synthesis in vitro post treatment of NAMPT inhibitor FK866. For some reasons such as differences in sex, age, and/or basal levels of cellular NAD+ availability, there are various inconclusive results regarding the impacts of NAD+ metabolism on adipocytes in the adipocyte-specific NAMPT-deficient mouse model or in vitro cell models. Further investigation on the effects of NAD+ supplementation and the distinct functions of NAMPT in adipocytes is still needed. 6. Conclusion The importance of NAD metabolism in WAT has been highlighted. NAD has tissue-specific roles. Specifically, WAT may be one of the direct target for NAD supplementation. Supplementation with NAD+ precursors can reduce fat accumulation and inflammation in adipose tissue. Reference Kwon SY, Park YJ. Function of NAD metabolism in white adipose tissue: lessons from mouse models. Adipocyte. 2024;13(1):2313297. doi:10.1080/21623945.2024.2313297 About BONTAC BONTAC has been dedicated to the R&D, manufacture and sale of raw materials for coenzyme and natural products since 2012, with self-owned factories, over 170 global patents as well as strong R&D team consisting of Doctors and Masters. BONTAC has rich R&D experience and advanced technology in the biosynthesis of NAD and its precursors (eg. NMN and NR), with various forms to be selected (eg. endoxin-free IVD-grade NAD, Na-free or Na-containing NAD; NR-CL or NR-Malate). High quality and stable supply of products can be better ensured here with the exclusive Bonpure seven-step purification technology and Bonzyme Whole-enzymatic method. Disclaimer 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. Under no circumstances will BONTAC be held responsible or liable in any way for any claims, damages, losses, expenses, costs or liabilities whatsoever (including, without limitation, any direct or indirect damages for loss of profits, business interruption or loss of information) resulting or arising directly or indirectly from your reliance on the information and material on this website.
The Miraculous Potency of NR-CL on Mitigating Ischemia-induced Hippocampal Damage and Maintaining Cognitive Function
1 Introduction Nicotinamide riboside (NR), a derivative of vitamin B3, is a new type of bioactive substance, which can be generated by binding a carbohydrate molecular ribose with nicotinamide (also known as niacin or vitamin B3). Nicotinamide riboside chloride (NRC/NR-CL) is a chloride salt form of NR. In daily life, NR-CL can be taken from NR supplements and food such as meat, fish and cereals. A recent study has revealed that NR-CL protects the hippocampus and ultimately promotes the recovery of cognitive function after brain ischemia. 2. The ameliorating impact of NRC upon ischemia-induced cognitive deficits Ischemia-induced cognitive deficits are ameliorated post NRC treatment. Specifically, NRC treatment improves the learning ability of mice, as evidenced by the shorter latency and the decreased path length. The hippocampal protection provided by NRC contributes to the recovery of spatial learning and memory after the ischemic insult. Figure 1 Acute NRC treatment potentiates cognitive recovery after ischemia 3. Reduction of the infarct volume in the hippocampus post acute NRC treatment After ischemia, there are deformed cell bodies, condensed nuclear chromatin, increased intracellular cell gaps, loosened cell arrangements and blurred visible staining in the damaged pyramidal neurons. NRC treatment partially offsets these morphological changes. Figure 2 Acute NRC treatment reduces the hippocampal infarct volume. 4. Recovery of neuronal damage in the hippocampus post acute NRC treatment After ischemia, brain damage emerges due to energy crisis-induced mitochondrial dysfunction, followed by the cell loss and neuronal apoptosis. NRC treatment leads to an increase in the number of positive cells, signifying the recovery of local neuronal loss. Figure 3 Acute NRC treatment attenuates neuronal loss in the hippocampus. 5. Upregulation of NAD and ATP levels in the hippocampus post acute NRC treatment By repleshing the production of NAD, acute treatment with NRC, to some extent, can salvage the energy supply in the hippocampus, which conspicuously enhances the recovery of ATP level. 6. Conclusion Collectively, acute NRC treatment increases the energy supply and reduces the neuronal loss to protect the hippocampus, thereby facilitating the recovery of cognitive function. NR-CL (ie. NRC) is a very promising component of health care products and has a wide range of application prospects. Before use, one should follow the guidance of professionals. At the same time, attention should be paid to reasonable intake and safe use to avoid the adverse effects of excessive use. References Cheng, Yin-Hong et al. “Acute Treatment with Nicotinamide Riboside Chloride Reduces Hippocampal Damage and Preserves the Cognitive Function of Mice with Ischemic Injury.” Neurochemical research vol. 47,8 (2022): 2244-2253. doi:10.1007/s11064-022-03610-3 Product advantages and features of BONTAC NR-CL * Bonzyme Whole-enzymatic method (environmental-friendly; no harmful solvent residues) * Unique Bonpure seven-step purification technology, with higher product content and higher conversion rate * Self-owned factories and a number of international certifications to ensure high quality and stable supply of products * One-stop customized service for product solution Disclaimer 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. Under no circumstances will BONTAC be held responsible or liable in any way for any claims, damages, losses, expenses, costs or liabilities whatsoever (including, without limitation, any direct or indirect damages for loss of profits, business interruption or loss of information) resulting or arising directly or indirectly from your reliance on the information and material on this website.
Amelioration of Myocardial I/R Injury with NR via Autophagy and Oxidative Stress
Introduction Myocardial ischemia-reperfusion (I/R) injury has emerged as an urgent clinical issue that may offset the benefits of reperfusion therapy and even worsen the prognosis of acute myocardial infarction, a severe cardiovascular disease with significant mortality and morbidity. Nicotinamide riboside (NR), a nicotinamide adenine dinucleotide (NAD+) intermediate, has been unveiled to hold great therapeutic potential in myocardial I/R injury. About myocardial I/R injury Myocardial I/R injury refers to the damaging effects on cardiomyocytes or heart tissues following ischemia and the regaining of blood perfusion or oxygen supply, with characteristics of cell swelling, contracture of myofibrils, and disruption of the sarcolemma in myocardium. The mechanisms of myocardial I/R injury are extremely complex, chiefly involving cellular and molecular biological events such as cellular oxidative stress, intracellular calcium overload, mitochondrial dysfunction, inflammatory response, apoptosis and autophagy. Strikingly, autophagy and oxidative stress have been perceived as vital factors in the treatment of myocardial I/R injury. The alleviating effects of NR on myocardial I/R injury in mice NR can improve the cardiac function of mice with myocardial I/R injury, and reduce the generation of myocardial injury- and oxidative stress-associated biomarkers. Herein, the optimal concentration of NR for protection against H/R injury is 10 mM. In vivo, NR diminishes the area of myocardial ischemic infarction, alleviates pathological myocardial changes, decreases inflammatory cell infiltration, and attenuates the levels of mitochondrial reactive oxygen species (ROS) as well as creatine kinase myocardial band (CK-MB). In vitro, NR pretreatment lessens the levels of lactate dehydrogenase, CK-MB, malondialdehyde, superoxide dismutase and ROS, as well as the mortality of H9c2 cells after the induction of hypoxia/reoxygenation (H/R) injury. The significance of Sirt 1 pathway in the regulation of autophagy by NR Excessive autophagy can exacerbate I/R injury, giving rise to an increase in cardiomyocyte apoptosis and greater cardiac dysfunction. Noteworthily, NR can lead to the activation of Sirt 1, an NAD+-dependent enzyme, to protect the H9c2 cells against excessive autophagy, thereby alleviating the myocardial I/R injury. Post NR pre-treatment, the levels of autophagy-related proteins (Beclin 1, P62 and LC3II/LC3I) are apparently downregulated in the H9c2 cells challenged with H/R. Remarkably, the supplement of Sirt 1 inhibitor EX527 overtly attenuates NR-induced reduction in the expression levels of autophagy-related proteins under H/R conditions, hinting the significance of Sirt 1 in the regulation of autophagy by NR. Conclusion The myocardial I/R injury can be ameliorated by regulating the autophagy and oxidative stress with NR. On the one hand, NR can directly participate in oxidative reduction to lessen the level of oxidative stress in cardiomyocytes. On the other hand, NR can protect cardiomyocytes against excessive autophagy, which is possibly accomplished by increasing the NAD+ content in the body via the Sirt 1 pathway. Reference Yuan C, Yang H, Lan W, et al. Nicotinamide ribose ameliorates myocardial ischemia/reperfusion injury by regulating autophagy and regulating oxidative stress. Exp Ther Med. 2024;27(5):187. doi:10.3892/etm.2024.12475 BONTAC NR BONTAC is one of the few suppliers in China that can launch mass production of raw materials for NR, with self-owned factory and professional R&D team. Up till now, there are 173 BONTAC patents. BONTAC provides one-stop service for customized products. Both malate and chloride salt forms of NR are available. By dirt of unique Bonpure seven-step purification technology and Bonzyme Whole-enzymatic method, the product content and conversion rate can be maintained in a higher level. The purity of BONTAC NR can reach above 97%. Our products are subjected to strict third-party self-inspection, which are worth of trustworthy. Disclaimer This article is based on the reference in the academic journal. The relevant information is provided 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. Under no circumstances will BONTAC be held responsible or liable in any way for any claims, damages, losses, expenses, costs or liabilities whatsoever (including, without limitation, any direct or indirect damages for loss of profits, business interruption or loss of information) resulting or arising directly or indirectly from your reliance on the information and material on this website.