Category: 1094-61-7

Physicochemical, Nutritional Properties and Metabolomics Analysis Fat Deposition Mechanism of Chahua Chicken Number 2 and Yao Chicken was written by Liu, Yong;Liang, Shuangmin;Wang, Kun;Zi, Xiannian;Zhang, Ru;Wang, Guangzheng;Kang, Jiajia;Li, Zijian;Dou, Tengfei;Ge, Changrong. And the article was included in Genes in 2022.Recommanded Product: ((2R,3S,4R,5R)-5-(3-Carbamoylpyridin-1-ium-1-yl)-3,4-dihydroxytetrahydrofuran-2-yl)methyl hydrogen phosphate The following contents are mentioned in the article:

Poultry is an important dietary source of animal protein, accounting for approx. 30% of global meat consumption. Because of its low price, low fat and cholesterol content, and no religious restrictions, chicken is considered a widely available healthy meat. Chahua chicken Number 2 is a synthetic breed of Chahua chicken derived from five generations of specialized strain breeding. In this study, Chahua chicken Number 2 (CH) and Yao chicken (Y) were used as the research objects to compare the differences in physicochem. and nutritional indicators of meat quality between the two chicken breeds, and metabolomics was used to analyze the differences in metabolites and lipid metabolism pathways and to explore the expression of genes involved in adipogenesis. The phys. index and nutritional value of CH are better than that of Y, and the chem. index of Y is better than that of CH. However, the chem. index results of CH are also within the normal theor. value range. Comprehensive comparison shows that the meat quality of CH is relatively good. Metabolomics anal. showed that CH and Y had 85 different metabolites, and the differential metabolites were mainly classified into eight categories. KEGG pathway enrichment anal. revealed 13 different metabolic pathways. The screened PPARG, FABP3, ACSL5, FASN, UCP3 and SC5D were neg. correlated with muscle fat deposition, while PPARα, ACACA and ACOX1 were pos. correlated with muscle fat deposition. The meat quality of CH was better than Y. The metabolites and metabolic pathways obtained by metabonomics anal. mainly involved the metabolism of amino acids and fatty acids, which were consistent with the differences in meat quality between the two breeds and the contents of precursors affecting flavor. The screened genes were associated with fatty deposition in poultry. This study involved multiple reactions and reactants, such as ((2R,3S,4R,5R)-5-(3-Carbamoylpyridin-1-ium-1-yl)-3,4-dihydroxytetrahydrofuran-2-yl)methyl hydrogen phosphate (cas: 1094-61-7Recommanded Product: ((2R,3S,4R,5R)-5-(3-Carbamoylpyridin-1-ium-1-yl)-3,4-dihydroxytetrahydrofuran-2-yl)methyl hydrogen phosphate).

((2R,3S,4R,5R)-5-(3-Carbamoylpyridin-1-ium-1-yl)-3,4-dihydroxytetrahydrofuran-2-yl)methyl hydrogen phosphate (cas: 1094-61-7) belongs to amides. Compared to amines, amides are very weak bases and do not have clearly defined acid–base properties in water. On the other hand, amides are much stronger bases than esters, aldehydes, and ketones. Ionic, or saltlike, amides are strongly alkaline compounds ordinarily made by treating ammonia, an amine, or a covalent amide with a reactive metal such as sodium.Recommanded Product: ((2R,3S,4R,5R)-5-(3-Carbamoylpyridin-1-ium-1-yl)-3,4-dihydroxytetrahydrofuran-2-yl)methyl hydrogen phosphate

Referemce:
Amide – Wikipedia,
Amide – an overview | ScienceDirect Topics

NAMPT-mediated NAD⁺ biosynthesis suppresses activation of hepatic stellate cells and protects against CCl₄-induced liver fibrosis in mice was written by Xu, Lin;Yang, Chenyan;Ma, Jie;Zhang, Xinge;Wang, Qingzhi;Xiong, Xiwen. And the article was included in Human & Experimental Toxicology in 2021.Safety of ((2R,3S,4R,5R)-5-(3-Carbamoylpyridin-1-ium-1-yl)-3,4-dihydroxytetrahydrofuran-2-yl)methyl hydrogen phosphate The following contents are mentioned in the article:

Nicotinamide phosphoribosyltransferase (NAMPT) catalyzes the rate-limiting step in the salvage pathway of mammalian NAD (NAD⁺) biosynthesis. Through its NAD⁺-biosynthetic activity, NAMPT is able to regulate the development of hepatic steatosis and inflammation induced by diet or alc. However, the roles NAMPT plays in the development of liver fibrosis remain obscure. To investigate the roles of NAMPT-mediated NAD⁺ biosynthesis in hepatic stellate cell (HSC) activation and liver fibrosis. Realtime RT-PCR and western blot analyses were performed to analyze the expression of profibrogenic genes. Sirius red staining was conducted to examine the fibrosis in liver. Mouse liver fibrosis was induced by i.p. injection of carbon tetrachloride (CCl₄) 2 times a week for 6 wk. Adenovirus-mediated NAMPT overexpression or NMN (NMN) administration was carried out to study the effects of elevation of NAD⁺ levels on protecting CCl₄-induced liver fibrosis in mice. The LX2 cells or primary HSCs were used to study the role of NAMPT overexpression or NMN treatment in reducing profibrogenic gene expression in vitro. The CCl₄ administration suppresses NAMPT expression in liver and reduces hepatic NAD⁺ content. The Tgfβ1 treatment decreases intracellular NAD⁺ levels and NAMPT expression in LX2 cells. Adenovirus-mediated NAMPT overexpression augments liver NAD⁺ levels, inhibits HSC activation and alleviates CCl₄-induced liver fibrosis in mice. Administration of NMN also suppresses HSC activation and protects against CCl₄-induced liver fibrosis in mice. The NAMPT-mediated NAD⁺ biosynthesis inhibits HSC activation and protects against CCl₄-induced liver fibrosis. This study involved multiple reactions and reactants, such as ((2R,3S,4R,5R)-5-(3-Carbamoylpyridin-1-ium-1-yl)-3,4-dihydroxytetrahydrofuran-2-yl)methyl hydrogen phosphate (cas: 1094-61-7Safety of ((2R,3S,4R,5R)-5-(3-Carbamoylpyridin-1-ium-1-yl)-3,4-dihydroxytetrahydrofuran-2-yl)methyl hydrogen phosphate).

((2R,3S,4R,5R)-5-(3-Carbamoylpyridin-1-ium-1-yl)-3,4-dihydroxytetrahydrofuran-2-yl)methyl hydrogen phosphate (cas: 1094-61-7) belongs to amides. Amides are pervasive in nature and technology. Proteins and important plastics like Nylons, Aramid, Twaron, and Kevlar are polymers whose units are connected by amide groups (polyamides); these linkages are easily formed, confer structural rigidity, and resist hydrolysis. Amides are not in general accessible by the direct condensation of amines with carboxylic acids for two reasons: first, both components are readily deactivated by a transfer of a proton from the acid to the amine and second, the hydroxy unit on the carbonyl of the acid is a relatively poor leaving group. Nevertheless, the formation of five- and six-membered rings is often surprisingly simple provided that other factors can be brought into play to assist in the condensation.Safety of ((2R,3S,4R,5R)-5-(3-Carbamoylpyridin-1-ium-1-yl)-3,4-dihydroxytetrahydrofuran-2-yl)methyl hydrogen phosphate

Referemce:
Amide – Wikipedia,
Amide – an overview | ScienceDirect Topics

NAMPT-mediated NAD⁺ biosynthesis suppresses activation of hepatic stellate cells and protects against CCl₄-induced liver fibrosis in mice was written by Xu, Lin;Yang, Chenyan;Ma, Jie;Zhang, Xinge;Wang, Qingzhi;Xiong, Xiwen. And the article was included in Human & Experimental Toxicology in 2021.Category: amides-buliding-blocks The following contents are mentioned in the article:

Nicotinamide phosphoribosyltransferase (NAMPT) catalyzes the rate-limiting step in the salvage pathway of mammalian NAD (NAD⁺) biosynthesis. Through its NAD⁺-biosynthetic activity, NAMPT is able to regulate the development of hepatic steatosis and inflammation induced by diet or alc. However, the roles NAMPT plays in the development of liver fibrosis remain obscure. To investigate the roles of NAMPT-mediated NAD⁺ biosynthesis in hepatic stellate cell (HSC) activation and liver fibrosis. Realtime RT-PCR and western blot analyses were performed to analyze the expression of profibrogenic genes. Sirius red staining was conducted to examine the fibrosis in liver. Mouse liver fibrosis was induced by i.p. injection of carbon tetrachloride (CCl₄) 2 times a week for 6 wk. Adenovirus-mediated NAMPT overexpression or NMN (NMN) administration was carried out to study the effects of elevation of NAD⁺ levels on protecting CCl₄-induced liver fibrosis in mice. The LX2 cells or primary HSCs were used to study the role of NAMPT overexpression or NMN treatment in reducing profibrogenic gene expression in vitro. The CCl₄ administration suppresses NAMPT expression in liver and reduces hepatic NAD⁺ content. The Tgfβ1 treatment decreases intracellular NAD⁺ levels and NAMPT expression in LX2 cells. Adenovirus-mediated NAMPT overexpression augments liver NAD⁺ levels, inhibits HSC activation and alleviates CCl₄-induced liver fibrosis in mice. Administration of NMN also suppresses HSC activation and protects against CCl₄-induced liver fibrosis in mice. The NAMPT-mediated NAD⁺ biosynthesis inhibits HSC activation and protects against CCl₄-induced liver fibrosis. This study involved multiple reactions and reactants, such as ((2R,3S,4R,5R)-5-(3-Carbamoylpyridin-1-ium-1-yl)-3,4-dihydroxytetrahydrofuran-2-yl)methyl hydrogen phosphate (cas: 1094-61-7Category: amides-buliding-blocks).

((2R,3S,4R,5R)-5-(3-Carbamoylpyridin-1-ium-1-yl)-3,4-dihydroxytetrahydrofuran-2-yl)methyl hydrogen phosphate (cas: 1094-61-7) belongs to amides. In primary and secondary amides, the presence of N–H dipoles allows amides to function as H-bond donors as well. Thus amides can participate in hydrogen bonding with water and other protic solvents; the oxygen atom can accept hydrogen bonds from water and the N–H hydrogen atoms can donate H-bonds. Ionic, or saltlike, amides are strongly alkaline compounds ordinarily made by treating ammonia, an amine, or a covalent amide with a reactive metal such as sodium.Category: amides-buliding-blocks

Referemce:
Amide – Wikipedia,
Amide – an overview | ScienceDirect Topics

The role of NAD metabolism in neuronal differentiation was written by Neves, Diogo;Goodfellow, Brian J.;Vieira, Sandra I.;Silva, Raquel M.. And the article was included in Neurochemistry International in 2022.Electric Literature of C11H15N2O8P The following contents are mentioned in the article:

NAD (NAD) metabolism is involved in redox and non-redox reactions that regulate several processes including differentiation of cells of different origins. Here, the role of NAD metabolism in neuronal differentiation, which remains elusive so far, was investigated. A protein-protein interaction network between neurotrophin signaling and NAD metabolic pathways was built. Expression of NAD biosynthetic enzymes in SH-SY5Y cells during retinoic acid (RA)/brain derived neurotrophic factor (BDNF) differentiation, was evaluated. The effects of NAD biosynthetic enzymes QPRT and NAPRT inhibition in neurite outgrowth, cell viability, NAD availability and histone deacetylase (HDAC) activity, were analyzed in RA- and BDNF-differentiated cells. Bioinformatics anal. revealed the interaction between NAD biosynthetic enzyme NMNAT1 and NTRK2, a receptor activated by RA/BDNF sequential treatment. Differences were found in the expression of NAD biosynthetic enzymes during neuronal differentiation, namely, increased QPRT gene expression along the course of RA/BDNF treatment and NAPRT protein expression after a 5-day treatment with RA. QPRT inhibition in BDNF-differentiated SH-SY5Y cells resulted in less neuritic length per cell, decreased expression of the neuronal marker β-III Tubulin and also decreased NAD+ levels and HDAC activity. NAPRT inhibition had no effect in neuritic length per cell, NAD+ levels and HDAC activity. Of note, NAD supplementation along with RA, but not with BDNF, resulted in considerable cell death. Taken together, our results show the involvement of NAD metabolism in neuronal differentiation, specifically, the importance of QPRT-mediated NAD biosynthesis in BDNF-associated SH-SY5Y differentiation and suggest addnl. roles for NAPRT beyond NAD production in RA-differentiated cells. This study involved multiple reactions and reactants, such as ((2R,3S,4R,5R)-5-(3-Carbamoylpyridin-1-ium-1-yl)-3,4-dihydroxytetrahydrofuran-2-yl)methyl hydrogen phosphate (cas: 1094-61-7Electric Literature of C11H15N2O8P).

((2R,3S,4R,5R)-5-(3-Carbamoylpyridin-1-ium-1-yl)-3,4-dihydroxytetrahydrofuran-2-yl)methyl hydrogen phosphate (cas: 1094-61-7) belongs to amides. In primary and secondary amides, the presence of N–H dipoles allows amides to function as H-bond donors as well. Thus amides can participate in hydrogen bonding with water and other protic solvents; the oxygen atom can accept hydrogen bonds from water and the N–H hydrogen atoms can donate H-bonds. Amides can be freed from solvent or water by drying below their melting points. These purifications can also be used for sulfonamides and acid hydrazides.Electric Literature of C11H15N2O8P

Referemce:
Amide – Wikipedia,
Amide – an overview | ScienceDirect Topics

Effects of temperature on growth performance and metabolism of juvenile sea bass (Dicentrarchus labrax) was written by Zhou, Cheng;Zhang, Zhi-qiang;Zhang, Lei;Liu, Ying;Liu, Peng-fei. And the article was included in Aquaculture in 2021.COA of Formula: C11H15N2O8P The following contents are mentioned in the article:

The European sea bass (Dicentrarchus labrax) has become an increasingly important aquaculture species due to the rapid expansion of farming in China and its com. popularity in Asia. A 60 day growth trial was conducted to investigate the impact of temperature on growth and ingestion performance and metabolism of the European sea bass (Dicentrarchus labrax). Juvenile European sea bass were stocked in triplicate at 3 temperature conditions (10°, 15°, and 20°). The specific growth rate and feeding rate of European sea bass in both 10° and 15° were all significantly lower than fish in 20° (P < 0.05). The feed conversion rate of European sea bass was 20° > 15° (P > 0.05), and 20° > 10° (P < 0.05). We measured the levels of muscle metabolites of European sea bass, using liquid chromatog. with tandem mass spectrometry-(LC-MS/MS) and compared the data among groups using principal component anal. and orthogonal partial least-squares discriminant anal. (OPLS-DA). We also conducted Kyoto Encyclopedia of Genes and Genomes (KEGG) metabolic pathway anal. OPLS-DA clearly discriminated the muscle metabolites of European sea bass under the three temperature conditions. The important differential metabolites mainly included β-NMN, nicotinic acid adenine dinucleotide, nicotinic acid, UDP-glucose, glycerophosphatidylcholine, (±)-17-hydroxy-4Z, 7Z, 10Z, 13Z, 15E, 19Z-docosahexaenoic acid, (±)-15-hydroxy-5Z, 8Z, 11Z, 13E, 17Z-eicosapentaenoic acid, γ-linolenic acid, L-serine, inositol, L-citrulline, and succinic acid. The KEGG metabolic pathway anal. showed that lipid metabolism, glucose metabolism, the tricarboxylic acid cycle, the urea cycle, and nicotinate and nicotinamide metabolism may closely related to temperature conditions. The findings of this research suggest that the growth and food intake of European sea bass can be promoted and production can be improved at a culture temperature of 20°. Our results provide a theor. basis and tech. guidance for formulating temperature control strategies for industrial recirculating aquaculture of European sea bass. This study involved multiple reactions and reactants, such as ((2R,3S,4R,5R)-5-(3-Carbamoylpyridin-1-ium-1-yl)-3,4-dihydroxytetrahydrofuran-2-yl)methyl hydrogen phosphate (cas: 1094-61-7COA of Formula: C11H15N2O8P).

((2R,3S,4R,5R)-5-(3-Carbamoylpyridin-1-ium-1-yl)-3,4-dihydroxytetrahydrofuran-2-yl)methyl hydrogen phosphate (cas: 1094-61-7) belongs to amides. Amides can be viewed as a derivative of a carboxylic acid RC(=O)OH with the hydroxyl group –OH replaced by an amine group −NR′R″; or, equivalently, an acyl (alkanoyl) group RC(=O)− joined to an amine group. Amides are not in general accessible by the direct condensation of amines with carboxylic acids for two reasons: first, both components are readily deactivated by a transfer of a proton from the acid to the amine and second, the hydroxy unit on the carbonyl of the acid is a relatively poor leaving group. Nevertheless, the formation of five- and six-membered rings is often surprisingly simple provided that other factors can be brought into play to assist in the condensation.COA of Formula: C11H15N2O8P

Referemce:
Amide – Wikipedia,
Amide – an overview | ScienceDirect Topics

SL010110, a lead compound, inhibits gluconeogenesis via SIRT2-p300-mediated PEPCK1 degradation and improves glucose homeostasis in diabetic mice was written by Ren, Yu-ran;Ye, Yang-liang;Feng, Ying;Xu, Ti-fei;Shen, Yu;Liu, Jia;Huang, Su-ling;Shen, Jian-hua;Leng, Ying. And the article was included in Acta Pharmacologica Sinica in 2021.Electric Literature of C11H15N2O8P The following contents are mentioned in the article:

Abstract: Suppression of excessive hepatic gluconeogenesis is an effective strategy for controlling hyperglycemia in type 2 diabetes (T2D). In the present study, we screened our compounds library to discover the active mols. inhibiting gluconeogenesis in primary mouse hepatocytes. We found that SL010110 (5-((4-allyl-2-methoxyphenoxy) methyl) furan-2-carboxylic acid) potently inhibited gluconeogenesis with 3μM and 10μM leading to a reduction of 45.5% and 67.5%, resp. Moreover, SL010110 caused suppression of gluconeogenesis resulted from downregulating the protein level of phosphoenolpyruvate carboxykinase 1 (PEPCK1), but not from affecting the gene expressions of PEPCK, glucose-6-phosphatase, and fructose-1,6-bisphosphatase. Furthermore, SL010110 increased PEPCK1 acetylation, and promoted PEPCK1 ubiquitination and degradation SL010110 activated p300 acetyltransferase activity in primary mouse hepatocytes. The enhanced PEPCK1 acetylation and suppressed gluconeogenesis caused by SL010110 were blocked by C646, a histone acetyltransferase p300 inhibitor, suggested that SL010110 inhibited gluconeogenesis by activating p300. SL010110 decreased NAD⁺/NADH ratio, inhibited SIRT2 activity, and further promoted p300 acetyltransferase activation and PEPCK1 acetylation. These effects were blocked by NMN, an NAD⁺ precursor, suggested that SL010110 inhibited gluconeogenesis by inhibiting SIRT2, activating p300, and subsequently promoting PEPCK1 acetylation. In type 2 diabetic ob/ob mice, single oral dose of SL010110 (100 mg/kg) suppressed gluconeogenesis accompanied by the suppressed hepatic SIRT2 activity, increased p300 activity, enhanced PEPCK1 acetylation and degradation Chronic oral administration of SL010110 (15 or 50 mg/kg) significantly reduced the blood glucose levels in ob/ob and db/db mice. This study reveals that SL010110 is a lead compound with a distinct mechanism of suppressing gluconeogenesis via SIRT2-p300-mediated PEPCK1 degradation and potent anti-hyperglycemic activity for the treatment of T2D. This study involved multiple reactions and reactants, such as ((2R,3S,4R,5R)-5-(3-Carbamoylpyridin-1-ium-1-yl)-3,4-dihydroxytetrahydrofuran-2-yl)methyl hydrogen phosphate (cas: 1094-61-7Electric Literature of C11H15N2O8P).

((2R,3S,4R,5R)-5-(3-Carbamoylpyridin-1-ium-1-yl)-3,4-dihydroxytetrahydrofuran-2-yl)methyl hydrogen phosphate (cas: 1094-61-7) belongs to amides. The amide group is called a peptide bond when it is part of the main chain of a protein, and an isopeptide bond when it occurs in a side chain, such as in the amino acids asparagine and glutamine. In simple aromatic amides, fragmentation occurs on both sides of the carbonyl group. If a hydrogen is available in N-substituted aromatic amides, it tends to migrate and form an aromatic amine and the loss of a ketene.Electric Literature of C11H15N2O8P

Referemce:
Amide – Wikipedia,
Amide – an overview | ScienceDirect Topics

SL010110, a lead compound, inhibits gluconeogenesis via SIRT2-p300-mediated PEPCK1 degradation and improves glucose homeostasis in diabetic mice was written by Ren, Yu-ran;Ye, Yang-liang;Feng, Ying;Xu, Ti-fei;Shen, Yu;Liu, Jia;Huang, Su-ling;Shen, Jian-hua;Leng, Ying. And the article was included in Acta Pharmacologica Sinica in 2021.Name: ((2R,3S,4R,5R)-5-(3-Carbamoylpyridin-1-ium-1-yl)-3,4-dihydroxytetrahydrofuran-2-yl)methyl hydrogen phosphate The following contents are mentioned in the article:

Abstract: Suppression of excessive hepatic gluconeogenesis is an effective strategy for controlling hyperglycemia in type 2 diabetes (T2D). In the present study, we screened our compounds library to discover the active mols. inhibiting gluconeogenesis in primary mouse hepatocytes. We found that SL010110 (5-((4-allyl-2-methoxyphenoxy) methyl) furan-2-carboxylic acid) potently inhibited gluconeogenesis with 3μM and 10μM leading to a reduction of 45.5% and 67.5%, resp. Moreover, SL010110 caused suppression of gluconeogenesis resulted from downregulating the protein level of phosphoenolpyruvate carboxykinase 1 (PEPCK1), but not from affecting the gene expressions of PEPCK, glucose-6-phosphatase, and fructose-1,6-bisphosphatase. Furthermore, SL010110 increased PEPCK1 acetylation, and promoted PEPCK1 ubiquitination and degradation SL010110 activated p300 acetyltransferase activity in primary mouse hepatocytes. The enhanced PEPCK1 acetylation and suppressed gluconeogenesis caused by SL010110 were blocked by C646, a histone acetyltransferase p300 inhibitor, suggested that SL010110 inhibited gluconeogenesis by activating p300. SL010110 decreased NAD⁺/NADH ratio, inhibited SIRT2 activity, and further promoted p300 acetyltransferase activation and PEPCK1 acetylation. These effects were blocked by NMN, an NAD⁺ precursor, suggested that SL010110 inhibited gluconeogenesis by inhibiting SIRT2, activating p300, and subsequently promoting PEPCK1 acetylation. In type 2 diabetic ob/ob mice, single oral dose of SL010110 (100 mg/kg) suppressed gluconeogenesis accompanied by the suppressed hepatic SIRT2 activity, increased p300 activity, enhanced PEPCK1 acetylation and degradation Chronic oral administration of SL010110 (15 or 50 mg/kg) significantly reduced the blood glucose levels in ob/ob and db/db mice. This study reveals that SL010110 is a lead compound with a distinct mechanism of suppressing gluconeogenesis via SIRT2-p300-mediated PEPCK1 degradation and potent anti-hyperglycemic activity for the treatment of T2D. This study involved multiple reactions and reactants, such as ((2R,3S,4R,5R)-5-(3-Carbamoylpyridin-1-ium-1-yl)-3,4-dihydroxytetrahydrofuran-2-yl)methyl hydrogen phosphate (cas: 1094-61-7Name: ((2R,3S,4R,5R)-5-(3-Carbamoylpyridin-1-ium-1-yl)-3,4-dihydroxytetrahydrofuran-2-yl)methyl hydrogen phosphate).

((2R,3S,4R,5R)-5-(3-Carbamoylpyridin-1-ium-1-yl)-3,4-dihydroxytetrahydrofuran-2-yl)methyl hydrogen phosphate (cas: 1094-61-7) belongs to amides. Amides are pervasive in nature and technology. Proteins and important plastics like Nylons, Aramid, Twaron, and Kevlar are polymers whose units are connected by amide groups (polyamides); these linkages are easily formed, confer structural rigidity, and resist hydrolysis. Amides can be freed from solvent or water by drying below their melting points. These purifications can also be used for sulfonamides and acid hydrazides.Name: ((2R,3S,4R,5R)-5-(3-Carbamoylpyridin-1-ium-1-yl)-3,4-dihydroxytetrahydrofuran-2-yl)methyl hydrogen phosphate

Referemce:
Amide – Wikipedia,
Amide – an overview | ScienceDirect Topics

Nicotinamide mononucleotide supplementation protects the intestinal function in aging mice and D-galactose induced senescent cells was written by Ru, Meng;Wang, Wanwan;Zhai, Zhenya;Wang, Ruxia;Li, Yumeng;Liang, Jiang;Kothari, Damini;Niu, Kaimin;Wu, Xin. And the article was included in Food & Function in 2022.Synthetic Route of C11H15N2O8P The following contents are mentioned in the article:

The NAD (NAD⁺) level shows a temporal decrease during the aging process, which has been deemed as an aging hallmark. NMN (NMN), a key NAD⁺ precursor, shows the potential to retard the age-associated functional decline in organs. In the current study, to explore whether NMN has an impact on the intestine during the aging process, the effects of NMN supplementation on the intestinal morphol., microbiota, and NAD⁺content, as well as its anti-inflammatory, anti-oxidative and barrier functions were investigated in aging mice and D-galactose (D-gal) induced senescent IPEC-J2 cells. The results showed that 4 mo of NMN administration had little impact on the colonic microbiota and NAD⁺ content in aging mice, while it significantly increased the jejunal NAD⁺ content and improved the jejunal structure i1ncluding increasing the villus length and shortening the crypt. Moreover, NMN supplementation significantly up-regulated the mRNA expression of SIRT3, SIRT6, nuclear factor E2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1), the catalytic subunit of glutamate-cysteine ligase (GCLC), superoxide dismutase 2 (SOD2), occludin, and claudin-1, but down-regulated the mRNA expression of tumor necrosis factor alpha (TNF-α). Specifically, in the D-gal induced senescent IPEC-J2 cells, 500μM NMN restored the increased mRNA expression of interleukin 6 (IL6ST), IL-1A, nuclear factor (NF-κB1), and claudin-1 to normal levels to some extent. Furthermore, NMN treatment significantly affected the mRNA expression of antioxidant enzymes including NQO1, GCLC, SOD 2 and 3, and GSH-PX1, 3 and 4. In addition, 200μM NMN enhanced the cell viability and total antioxidant capacity and lowered the reactive oxygen species level of senescent IPEC-J2 cells. Notably, NMN restored the down-regulated protein expression of occludin and claudin-1 induced by D-gal. The above data demonstrated the potential of NMN in ameliorating the structural and functional decline in the intestine during aging. This study involved multiple reactions and reactants, such as ((2R,3S,4R,5R)-5-(3-Carbamoylpyridin-1-ium-1-yl)-3,4-dihydroxytetrahydrofuran-2-yl)methyl hydrogen phosphate (cas: 1094-61-7Synthetic Route of C11H15N2O8P).

((2R,3S,4R,5R)-5-(3-Carbamoylpyridin-1-ium-1-yl)-3,4-dihydroxytetrahydrofuran-2-yl)methyl hydrogen phosphate (cas: 1094-61-7) belongs to amides. Amides include many other important biological compounds, as well as many drugs like paracetamol, penicillin and LSD. Low-molecular-weight amides, such as dimethylformamide, are common solvents. As a result of interactions such as these, the water solubility of amides is greater than that of corresponding hydrocarbons. These hydrogen bonds are also have an important role in the secondary structure of proteins.Synthetic Route of C11H15N2O8P

Referemce:
Amide – Wikipedia,
Amide – an overview | ScienceDirect Topics

Nicotinamide mononucleotide supplementation protects the intestinal function in aging mice and D-galactose induced senescent cells was written by Ru, Meng;Wang, Wanwan;Zhai, Zhenya;Wang, Ruxia;Li, Yumeng;Liang, Jiang;Kothari, Damini;Niu, Kaimin;Wu, Xin. And the article was included in Food & Function in 2022.Computed Properties of C11H15N2O8P The following contents are mentioned in the article:

The NAD (NAD⁺) level shows a temporal decrease during the aging process, which has been deemed as an aging hallmark. NMN (NMN), a key NAD⁺ precursor, shows the potential to retard the age-associated functional decline in organs. In the current study, to explore whether NMN has an impact on the intestine during the aging process, the effects of NMN supplementation on the intestinal morphol., microbiota, and NAD⁺content, as well as its anti-inflammatory, anti-oxidative and barrier functions were investigated in aging mice and D-galactose (D-gal) induced senescent IPEC-J2 cells. The results showed that 4 mo of NMN administration had little impact on the colonic microbiota and NAD⁺ content in aging mice, while it significantly increased the jejunal NAD⁺ content and improved the jejunal structure i1ncluding increasing the villus length and shortening the crypt. Moreover, NMN supplementation significantly up-regulated the mRNA expression of SIRT3, SIRT6, nuclear factor E2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1), the catalytic subunit of glutamate-cysteine ligase (GCLC), superoxide dismutase 2 (SOD2), occludin, and claudin-1, but down-regulated the mRNA expression of tumor necrosis factor alpha (TNF-α). Specifically, in the D-gal induced senescent IPEC-J2 cells, 500μM NMN restored the increased mRNA expression of interleukin 6 (IL6ST), IL-1A, nuclear factor (NF-κB1), and claudin-1 to normal levels to some extent. Furthermore, NMN treatment significantly affected the mRNA expression of antioxidant enzymes including NQO1, GCLC, SOD 2 and 3, and GSH-PX1, 3 and 4. In addition, 200μM NMN enhanced the cell viability and total antioxidant capacity and lowered the reactive oxygen species level of senescent IPEC-J2 cells. Notably, NMN restored the down-regulated protein expression of occludin and claudin-1 induced by D-gal. The above data demonstrated the potential of NMN in ameliorating the structural and functional decline in the intestine during aging. This study involved multiple reactions and reactants, such as ((2R,3S,4R,5R)-5-(3-Carbamoylpyridin-1-ium-1-yl)-3,4-dihydroxytetrahydrofuran-2-yl)methyl hydrogen phosphate (cas: 1094-61-7Computed Properties of C11H15N2O8P).

((2R,3S,4R,5R)-5-(3-Carbamoylpyridin-1-ium-1-yl)-3,4-dihydroxytetrahydrofuran-2-yl)methyl hydrogen phosphate (cas: 1094-61-7) belongs to amides. Because of the greater electronegativity of oxygen, the carbonyl (C=O) is a stronger dipole than the N–C dipole. The presence of a C=O dipole and, to a lesser extent a N–C dipole, allows amides to act as H-bond acceptors. Amides are stable compounds. The lower-melting members (such as acetamide) can be readily purified by fractional distillation. Most amides are solids which have low solubilities in water.Computed Properties of C11H15N2O8P

Referemce:
Amide – Wikipedia,
Amide – an overview | ScienceDirect Topics

Combination of nicotinamide mononucleotide and troxerutin induces full protection against doxorubicin-induced cardiotoxicity by modulating mitochondrial biogenesis and inflammatory response was written by Khosroshahi, Ahmad Jamei;Mokhtari, Behnaz;Badalzadeh, Reza. And the article was included in Molecular Biology Reports in 2022.Quality Control of ((2R,3S,4R,5R)-5-(3-Carbamoylpyridin-1-ium-1-yl)-3,4-dihydroxytetrahydrofuran-2-yl)methyl hydrogen phosphate The following contents are mentioned in the article:

Abstract: Background: Clin. application of doxorubicin (DOX) is restricted due to its cardiotoxicity, reinforcing the significance of exploring new strategies to counteract DOX-induced cardiotoxicity. The present work aimed to investigate the ameliorative impact of combination therapy with NMN (NMN) and troxerutin (TXR) on DOX-induced cardiotoxicity, with mitochondrial function/biogenesis and inflammatory response approach. Methods: Male Wistar rats (n = 30, 250-300 g) were divided into groups with/without DOX and/or NMN and TXR, alone or in combination. Rats underwent 6 consecutive i.p. injections of DOX (cumulative dose: 12 mg/kg). NMN (100 mg/kg/day; i.p.) and/or TXR (150 mg/kg/day; orally) were administered for 28 days before DOX challenge. Seven days following the last injection of DOX, evaluation of cardiac histopathol. changes, BNP and LDH levels, mitochondrial function (membrane potential, ROS generation, and ATP levels), expression of proteins involved in mitochondrial biogenesis (PGC-1α, NRF1, and TFAM), and inflammatory cytokines (TNF-α, IL-1β, and IL-6) was performed. Results: Combination of NMN and TXR significantly decreased the severity of histopathol. damages, and BNP and LDH levels (P < 0.01 to P < 0.001). It also restored mitochondrial functional endpoints, and expression of proteins involved in mitochondrial biogenesis (P < 0.05 to P < 0.001), and decreased inflammatory cytokines (P < 0.01 to P < 0.001). The pos. impacts of this combination therapy were more potent as compared to monotherapies. Conclusions: These findings shed new light on the understanding of additive properties of NMN/TXR combination therapy in protecting against DOX-induced cardiotoxicity. The cardioprotective effect of this combination therapy may be mediated in part through the restoration of mitochondrial function/biogenesis associated with the PGC-1α/NRF1/TFAM pathway, and suppression of inflammatory response. This study involved multiple reactions and reactants, such as ((2R,3S,4R,5R)-5-(3-Carbamoylpyridin-1-ium-1-yl)-3,4-dihydroxytetrahydrofuran-2-yl)methyl hydrogen phosphate (cas: 1094-61-7Quality Control of ((2R,3S,4R,5R)-5-(3-Carbamoylpyridin-1-ium-1-yl)-3,4-dihydroxytetrahydrofuran-2-yl)methyl hydrogen phosphate).

((2R,3S,4R,5R)-5-(3-Carbamoylpyridin-1-ium-1-yl)-3,4-dihydroxytetrahydrofuran-2-yl)methyl hydrogen phosphate (cas: 1094-61-7) belongs to amides. In primary and secondary amides, the presence of N–H dipoles allows amides to function as H-bond donors as well. Thus amides can participate in hydrogen bonding with water and other protic solvents; the oxygen atom can accept hydrogen bonds from water and the N–H hydrogen atoms can donate H-bonds. Amides can be freed from solvent or water by drying below their melting points. These purifications can also be used for sulfonamides and acid hydrazides.Quality Control of ((2R,3S,4R,5R)-5-(3-Carbamoylpyridin-1-ium-1-yl)-3,4-dihydroxytetrahydrofuran-2-yl)methyl hydrogen phosphate

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Amide – Wikipedia,
Amide – an overview | ScienceDirect Topics