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
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
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
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
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.
The Chinese name of NMNH is "reduced nicotinamide mononucleotide". NMNH is an amorphous yellow powder. NMNH increases NAD+ levels faster and at a higher concentration, on average 5 times that of NMN. NMNH has been industrialized and has a purity of ≥99%. It is available in two forms: free acid and sodium salt.
Introduction Intervertebral disc degeneration (IDD) is a frequently seen orthopedic disease, which is accompanied with excessive apoptosis of nucleus pulposus cells (NPCs) and degeneration of extracellular matrix (ECM), with main symptoms of pain and numbness in the waist, legs and feet, as well as inflammation on and around the surface of bone tissues. Strikingly, ginsenoside Rg3, the main active ingredient of ginseng, has been attested to exhibit anti-catabolic and anti-apoptotic effects in IL-1β-treated human NPCs and IDD rats by inactivating the p38 MAPK pathway. The risk factors for IDD IDD is generally associated with risk factors such as aging, excessive exercise, working environment, and genetics. As one ages, the amount of water in the body and in the intervertebral discs will be reduced accordingly. Intervertebral discs that lack moisture will lose their elastic function and become hard. Once there is any stimulation or pressure, the intervertebral disc may crack, leading to intervertebral disc injury. For instance, the mechanical trauma caused by excessive exercise and work may accelerate the fragility of disc and exacerbate IDD. Anti-catabolic and anti-apoptotic effects of ginsenoside Rg3 in IL-1β-treated human NPCs and IDD rats Ginsenoside Rg3 plays an anti-apoptotic role in IL-1β-treated human NPCs and IDD rats, as evidenced by the down-regulation of pro-apoptosis protein Bax and up-regulation of anti-apoptosis protein Bcl-2 in IL-1β-stimulated NPCs and IDD model rats. Besides, ginsenoside Rg3 represses ECM degradation in IL-1β-stimulated NPCs and intervertebral disc tissues of IDD rats, as attested by the decreased expression of ECM degradation-related factors MMPs (MMP2 and MMP3) and ADAMTSs (Adamts4, and Adamts5). Ginsenoside Rg3 exhibits anti-catabolic and anti-apoptotic effects in IL-1β-treated human NPCs. Ginsenoside Rg3 reduces apoptosis and catabolism in IDD rats. Alleviation of ginsenoside Rg3 in IDD via p38 MAPK pathway Ginsenoside Rg3 can alleviate NPC degeneration, recover the arrangement of annulus fibrous, and preserve more proteoglycan matrix via inactivating p38 MAPK pathway. In vitro, the fluorescence intensity of p38 is enhanced in IL-1β-stimulated NPCs, yet ginsenoside Rg3 offsets this promoting effect. In vivo, the phosphorylated p38 level is elevated in NPCs and the intervertebral disc tissues of IDD rats, while ginsenoside Rg3 works inversely. Ginsenoside Rg3 suppresses the IL-1β-stimulated p38 MAPK pathway in human NPCs Ginsenoside Rg3 inactivates the p38 MAPK pathway in IDD rats. Conclusion The anti-catabolic and anti-apoptotic effects of ginsenoside Rg3 in IL-1β treated human disc nucleus pulposus cells and in a rat model of disc degeneration are accomplished by inactivating the MAPK pathway, providing new clues on the treatment of IDD. Reference Chen J, Zhang B, Wu L, et al. Ginsenoside Rg3 exhibits anti-catabolic and anti-apoptotic effects in IL-1β treated human disc nucleus pulposus cells and in a rat model of disc degeneration by inactivating the MAPK pathway. Cell Mol Biol. 2024;70(1):233-238. doi:10.14715/cmb/2024.70.1.32 BONTAC Ginsenosides 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. BONTAC has rich R&D experience and advanced technology in the biosynthesis of rare ginsenosides Rh2/Rg3, with pure raw materials, higher conversion rate and higher content (up to 99%). One-stop service for customized product solution is available in BONTAC. With unique Bonzyme enzymatic synthesis technology, both S-type and R-type isomers can be accurately synthesized here, with stronger activity and precise targeting action. 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 responsible or liable in any way for any claims, damages, losses, expenses or costs resulting or arising directly or indirectly from your reliance on the information and material on this website.
1. Introduction The gut microbiota has long been regarded as one of the key elements contributing to the regulation of host health. Any changes in the composition or quality of the gut microbiota may have physiological consequences for the host. To determine the effect of sweetener stevia (also known as stevioside) on the gut microbiome of healthy population, the stool samples are collected from healthy participants who consume with or without five drops of the sweetener stevia twice daily. Following analyses of 16S rRNA sequencing method, no large-scale change is found in the gut microbiota post 12 weeks of consumption with stevia, hinting the safety of stevia. 2. Insignificant changes in the alpha or beta diversity following consumption of stevia It is discovered that there is no significant difference in alpha diversity (in terms of observed taxa, evenness and Shannon Index) and beta diversity (with regard to PCoA, PERMANOVA, and Jaccard Index) between groups. Nevertheless, PCoA plots shows strong separation along the x-axis. In addition, the community composition in each group is relatively even over time and equally diverse. 3. No clear difference in relative abundances of taxa At the genus level, relative abundances are similar between the control and stevia groups. No major difference is observed in relative abundances at the class, order and family level. Strikingly, butyricoccus is the only one identified taxon exhibiting significant difference at baseline, but not after 12 weeks of stevia consumption. Moreover, Collinsella and Aldercreutzia are two coprococcus species identified as explicitly different at baseline (one higher and one lower when comparing stevia vs. control), which however are significantly elevated after 12 weeks of consumption with stevia. 4. The safe intake volume of sweetener steviol glycosides In the European Food Safety Authority (EFSA), there is a Panel on Food Additives and Flavourings (FAF), which is responsible for evaluating the safety of food additives and establishing acceptable daily intake levels for safe use. Steviol glycosides, one of the extract from stevia, is evaluated by the FAF as well. In accordance to the latest toxicological test, this sweeter is not genotoxic and carcinogenic, without any adverse effects on the human reproductive system or growing children. The expert group has set the acceptable daily intake (ADI) of steviol glycosides at 4 milligrams per kilogram of body weight per day, which is consistent with the level determined by the Joint Expert Committee on Food Additives (JECFA) administered by the US Food and Agriculture Organization (FAO) and the World Health Organization (WHO). 5. Conclusion Regular, long-term consumption of stevia does not overtly alter the composition of the human gut microbiotia. Stevia can be safe as long as the intake volume is controlled appropriately. Reference Singh G, McBain AJ, McLaughlin JT, Stamataki NS. Consumption of the Non-Nutritive Sweetener Stevia for 12 Weeks Does Not Alter the Composition of the Human Gut Microbiota. Nutrients. 2024;16(2):296. Published 2024 Jan 18. doi:10.3390/nu16020296 BONTAC Stevia/Stevioside (RD) 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. Patent-grade Stevia Reb-D (US11312948B2 & ZL2018800019752) is availbale at BONTAC. High quality and stable supply of stevioside Reb-D 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.
1. Introduction In mammalian cells, the majority of NAD+ is produced from metabolites entering the NAD+ salvage pathway. Nicotinamide phosphoribosyltransferase (NAMPT) is the rate-limiting enzyme of the salvage pathway, which can convert nicotinamide (NAM) into nicotinamide mononucleotide (NMN). Neuronal NAMPT is important for pre-/post-synaptic NMJ function, and maintaining skeletal muscular function and structure. 2. The involvement of NAMPT in NAD+ salvage pathway NAMPT activity has a pivotal role in energy metabolism and homeostasis. NAMPT can condense nicotinamide (NAM) and 5-phosphoribosyl pyrophosphate (PRPP) into nicotinamide mononucleotide (NMN). NMN is subsequently synthesized into NAD+ by nicotinamide mononucleotide adenylyltransferase (NMNAT), the enzyme immediately after NAMPT. 3. The effect of NMN on partially reversing the NMJ impairments in NAMPT-/- cKO mice In the presence of NMN treatment, vesicle endocytosis/exocytosis is improved and endplate morphology is restored in Thy1-NAMPT-/-conditional knockout (cKO) mice. Also, loss of NAMPT in projection neurons impairs the endocytosis and exocytosis of synaptic vesicles at NMJs, but NMN can largely prevent these impairments. Furthermore, NMN treatment restores sarcomere alignment rather than mitochondrial morphology. 4. The underlying mechanism of NMN affecting NMJs The ameliorating effects of NMN on NMJs may be realized via NAMPT-mediated NAD+ salvage pathway, and this speculation is confirmed by the ameliorated synaptic vesicle cycling, endplate morphology, and muscle fiber structure and function post 2-week administration of the NAD+ precursor, NMN. 5. Conclusion Mechanically, the effects of NMN improving NMJ function, endplate morphology and muscular structure and contractility possibly involves NAMPT-mediated NAD+ salvage pathway. NMN holds a great promise as a therapeutic agent for skeletal muscle diseases. Reference Lundt S, Zhang N, Wang X, Polo-Parada L, Ding S. The effect of NAMPT deletion in projection neurons on the function and structure of neuromuscular junction (NMJ) in mice. Sci Rep. 2020;10(1):99. Published 2020 Jan 9. doi:10.1038/s41598-019-57085-4 BONTAC NMN 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 BOMNTAC are widely used in fields such as nutritional health, biomedicine, medical beauty, daily chemicals and green agriculture. 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.