Month: November 2022

NAMPT-dependent NAD⁺ salvage is crucial for the decision between apoptotic and necrotic cell death under oxidative stress was written by Nishida, Takuto;Naguro, Isao;Ichijo, Hidenori. And the article was included in Cell Death Discovery in 2022.Product Details of 1094-61-7 The following contents are mentioned in the article:

Oxidative stress is a state in which the accumulation of reactive oxygen species exceeds the capacity of cellular antioxidant systems. Both apoptosis and necrosis are observed under oxidative stress, and we have reported that these two forms of cell death are induced in H₂O₂-stimulated HeLa cells depending on the concentration of H₂O₂. Weak H₂O₂ stimulation induces apoptosis, while strong H₂O₂ stimulation induces necrosis. However, the detailed mechanisms controlling the switching between these forms of cell death depending on the level of oxidative stress remain elusive. Here, we found that NAD⁺ metabolism is a key factor in determining the form of cell death in H₂O₂-stimulated HeLa cells. Under both weak and strong H₂O₂ stimulation, intracellular NAD (NAD⁺) was depleted to a similar extent by poly (ADP-ribose) (PAR) polymerase 1 (PARP1)-dependent consumption. However, the intracellular NAD⁺ concentration recovered under weak H₂O₂ stimulation but not under strong H₂O₂ stimulation. NAD⁺ recovery was mediated by nicotinamide (NAM) phosphoribosyltransferase (NAMPT)-dependent synthesis via the NAD⁺ salvage pathway, which was suggested to be impaired only under strong H₂O₂ stimulation. Furthermore, downstream of NAD⁺, the dynamics of the intracellular ATP concentration paralleled those of NAD⁺, and ATP-dependent caspase-9 activation via apoptosome formation was thus impaired under strong H₂O₂ stimulation. Collectively, these findings suggest that NAD⁺ dynamics balanced by PARP1-dependent consumption and NAMPT-dependent production are important to determine the form of cell death activated under oxidative stress. 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: 1094-61-7Product Details of 1094-61-7).

((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. 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.Product Details of 1094-61-7

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

NAMPT-dependent NAD⁺ salvage is crucial for the decision between apoptotic and necrotic cell death under oxidative stress was written by Nishida, Takuto;Naguro, Isao;Ichijo, Hidenori. And the article was included in Cell Death Discovery 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:

Oxidative stress is a state in which the accumulation of reactive oxygen species exceeds the capacity of cellular antioxidant systems. Both apoptosis and necrosis are observed under oxidative stress, and we have reported that these two forms of cell death are induced in H₂O₂-stimulated HeLa cells depending on the concentration of H₂O₂. Weak H₂O₂ stimulation induces apoptosis, while strong H₂O₂ stimulation induces necrosis. However, the detailed mechanisms controlling the switching between these forms of cell death depending on the level of oxidative stress remain elusive. Here, we found that NAD⁺ metabolism is a key factor in determining the form of cell death in H₂O₂-stimulated HeLa cells. Under both weak and strong H₂O₂ stimulation, intracellular NAD (NAD⁺) was depleted to a similar extent by poly (ADP-ribose) (PAR) polymerase 1 (PARP1)-dependent consumption. However, the intracellular NAD⁺ concentration recovered under weak H₂O₂ stimulation but not under strong H₂O₂ stimulation. NAD⁺ recovery was mediated by nicotinamide (NAM) phosphoribosyltransferase (NAMPT)-dependent synthesis via the NAD⁺ salvage pathway, which was suggested to be impaired only under strong H₂O₂ stimulation. Furthermore, downstream of NAD⁺, the dynamics of the intracellular ATP concentration paralleled those of NAD⁺, and ATP-dependent caspase-9 activation via apoptosome formation was thus impaired under strong H₂O₂ stimulation. Collectively, these findings suggest that NAD⁺ dynamics balanced by PARP1-dependent consumption and NAMPT-dependent production are important to determine the form of cell death activated under oxidative stress. 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. 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. 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.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

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

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

The alkamide trans-pellitorine targets pparg via trpv1 and trpa1 to reduce lipid accumulation in developing 3t3-l1 adipocytes was written by Lieder, Barbara;Zaunschirm, Mathias;Holik, Ann-Katrin;Ley, Jakob P.;Hans, Joachim;Krammer, Gerhard E.;Somoza, Veronika. And the article was included in Frontiers in Pharmacology in 2017.Formula: C14H25NO The following contents are mentioned in the article:

Adipose tissue is an important endocrine organ in the human body. However, pathol. overgrowth is associated with chronic illness. Regulation of adipogenesis and maturation of adipocytes via bioactive compounds in our daily diet has been in focus of research in the past years and showed promising results for agonists of the ion channels transient receptor potential channel (TRP) V1 and A1. Here, we investigated the anti-adipogenic potential and underlying mechanisms of the alkamide trans-pellitorine present in Piper nigrum via TRPV1 and TRPA1 in 3T3-L1 cells. transpellitorine was found to suppress mean lipid accumulation, when applied during differentiation and maturation, but also during maturation phase solely of 3T3-L1 cells in a concentration range between 1 nM and 1 mM by up to 8.84 ± 4.97 or 7.49 ± 5.08%, resp. Blockage of TRPV1 using the specific inhibitor trans-tert-butyl-cyclohexanol demonstrated that the anti-adipogenic activity of transpellitorine depends on TRPV1. In addition, blockage of the TRPA1 channel using the antagonist AP-18 showed a TRPA1-dependent signaling in the early to intermediate stages of adipogenesis. On a mechanistic level, treatment with trans-pellitorine during adipogenesis led to reduced PPARg expression on gene and protein level via activation of TRPV1 and TRPA1, and increased expression of the microRNA mmu-let-7b, which has been associated with reduced PPARg levels. In addition, cells treated with transpellitorine showed decreased expression of the gene encoding for fatty acid synthase, increased expression of microRNA-103 and a decreased short-term fatty acid uptake on the functional level. In summary, these data point to an involvement of the TRPV1 and TRPA1 cation channels in the anti-adipogenic activity of trans-pellitorine via microRNAlet7b and PPARg. Since trans-pellitorine does not directly activate TRPV1 or TRPA1, an indirect modulation of the channel activity is assumed and warrants further investigation. This study involved multiple reactions and reactants, such as (2E,4E)-N-Isobutyldeca-2,4-dienamide (cas: 18836-52-7Formula: C14H25NO).

(2E,4E)-N-Isobutyldeca-2,4-dienamide (cas: 18836-52-7) belongs to amides. The solubilities of amides and esters are roughly comparable. Typically amides are less soluble than comparable amines and carboxylic acids since these compounds can both donate and accept hydrogen bonds. Tertiary amides, with the important exception of N,N-dimethylformamide, exhibit low solubility in water. The presence of the amide group –C(=O)N– is generally easily established, at least in small molecules. It can be distinguished from nitro and cyano groups in IR spectra. Amides exhibit a moderately intense νCO band near 1650 cm−1. By 1H NMR spectroscopy, CONHR signals occur at low fields. In X-ray crystallography, the C(=O)N center together with the three immediately adjacent atoms characteristically define a plane.Formula: C14H25NO

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

Pd(II) complexes with chelating N-(1-alkylpyridin-4(1H)-ylidene)amide (PYA) ligands: Synthesis, characterization and evaluation of anticancer activity was written by Zafar, Muhammad Naveed;Butt, Abdul Mannan;Chaudhry, Gul-e-Saba;Perveen, Fouzia;Nazar, Muhammad Faizan;Masood, Sara;Dalebrook, Andrew Francis;Mughal, Ehsan Ullah;Sumrra, Sajjad Hussain;Sung, Yeong Yik;Muhammad, Tengku Sifzizul Tengku;Wright, Leonard James. And the article was included in Journal of Inorganic Biochemistry in 2021.Quality Control of N1,N2-Di(pyridin-4-yl)oxalamide The following contents are mentioned in the article:

The bidentate N-(1-Alkylpyridin-4(1H)-ylidene)amide (PYA) pro-ligands [H₂L_Bn][Cl]₂ (2), and [H₂L_Me][TfO]₂ (3) were prepared by simple alkylation reactions of the known compound, N,N-di(pyridin-4-yl)oxalamide (H₂L, 1). The Pd(II) complexes, [Pd(L_Bn)₂][Cl]₂ (4), [Pd(L_Me)₂][Cl][TfO] (5), Pd(L_Bn)Cl₂ (6) and Pd(L_Me)Cl₂ (7) were synthesized through reactions between these pro-ligands and suitable Pd(II) substrates in the presence of base. The mol. structures of 3 and 6 were obtained by single crystal x-ray structure determinations Studies of the exptl. and computational DNA binding interactions of 1–7 revealed that overall 4 and 6 have the largest values for the binding parameters K_b and ΔG^o_b. The results showed a good correlation with the steric and electronic parameters obtained by quant. structure activity relation (QSAR) studies. In-vitro cytotoxicity studies against four different cell lines showed that the human breast cancer cell lines MCF-7, T47D and cervical cancer cell line HeLa had either higher or similar sensitivities towards 4, 6 and 2, resp., compared to cisplatin. In general, the cytotoxicity of the compounds, represented by IC₅₀ values, decreased in the order 4 > 6 > 2 > 5 > 3 > 1 > 7 in cancer cell lines. Apoptosis contributed significantly to the cytotoxic effects of these anticancer agents as evaluated by apoptosis studies. This study involved multiple reactions and reactants, such as N1,N2-Di(pyridin-4-yl)oxalamide (cas: 53118-43-7Quality Control of N1,N2-Di(pyridin-4-yl)oxalamide).

N1,N2-Di(pyridin-4-yl)oxalamide (cas: 53118-43-7) 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. 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.Quality Control of N1,N2-Di(pyridin-4-yl)oxalamide

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

A selective and sensitive UFLC-MS/MS method for the simultaneous determination of five alkaloids from Piper longum L. and its application in the pharmacokinetic study of 6-OHDA-induced Parkinson’s disease rats was written by Xu, Rongrong;Zhao, Wenwen;Yu, Lan;Chen, Qijun;Hu, Xiaolu;Ba, Yinying;Chen, Xiaoqing;Wang, Xing;Wu, Xia. And the article was included in RSC Advances in 2019.Recommanded Product: 18836-52-7 The following contents are mentioned in the article:

The alkaloids from Piper longum L. (PLA) mainly contain piperine (PPR), piperlongumine (PPL), Δα,β-dihydropiperlonguminine (DPPL), piperanine (PPRA) and pellitorine (PLTR), which have neuroprotective effects on a 6-OHDA-induced rat model of Parkinson’s disease (PD). To elucidate the pharmacokinetic profiles of these main compounds in PD rats, we developed a rapid, selective and sensitive ultra-fast liquid chromatog.-electronic spray ionization-tandem mass spectrometry (UFLC-ESI-MS/MS) method which was validated for the simultaneous determination of the 5 absorbed compounds in the plasma of 6-OHDA-induced PD rats. The plasma samples were pretreated using a protein precipitation method with methanol/acetonitrile (1 : 1, volume/volume). The analytes and internal standard (IS) were separated on a Phenomenex Gemini C18 column using gradient elution with a mobile phase consisting of acetonitrile and a 0.1% formic acid aqueous solution at a flow rate of 0.5 mL min^-1. The total chromatog. running time was 4.5 min. The detection was performed with pos. electrospray ionization (ESI) using the multiple reaction monitoring (MRM) mode of transitions at m/z 286.2 → 201.2, m/z 274.2 → 201.2, m/z 276.2 → 135.1, m/z 288.2 → 135.1, m/z 224.1 → 168.2, and m/z 472.1 → 436.1 for PPR, PPL, DPPL, PPRA, PLTR and IS, resp. All five analytes showed excellent linearity (R > 0.995) within the concentration range of 0.20-5000 ng mL^-1. The established method was then applied to investigate the pharmacokinetics of multi-components (PPR, PPL, DPPL, PPRA and PLTR) in PD rats after oral administration of PLA. The results showed that no obvious differences were observed in the pharmacokinetic parameters of PPR, PPL, DPPL, PPRA and PLTR in PD rats compared with those in sham rats after oral administration of PLA except for MRTs for PPR, PPL and PLTR. Addnl., the activities of superoxide dismutase (SOD) were related to the concentrations of the multi-components in plasma. This study involved multiple reactions and reactants, such as (2E,4E)-N-Isobutyldeca-2,4-dienamide (cas: 18836-52-7Recommanded Product: 18836-52-7).

(2E,4E)-N-Isobutyldeca-2,4-dienamide (cas: 18836-52-7) 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. 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.Recommanded Product: 18836-52-7

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

Pellitorine, an extract of Tetradium daniellii, is an antagonist of the ion channel TRPV1 was written by Olah, Zoltan;Redei, Dora;Pecze, Laszlo;Vizler, Csaba;Josvay, Katalin;Forgo, Peter;Winter, Zoltan;Dombi, Gyorgy;Szakonyi, Gerda;Hohmann, Judit. And the article was included in Phytomedicine in 2017.Recommanded Product: (2E,4E)-N-Isobutyldeca-2,4-dienamide The following contents are mentioned in the article:

Transient Receptor Potential Vanilloid 1 (TRPV1) confers noxious heat and inflammatory pain signals in the peripheral nervous system. Clin. trial of resiniferatoxin from Euphorbia species is successfully aimed at TRPV1 in cancer pain management and heading toward new selective painkiller status that further validates this target for drug discovery efforts. Evodia species, used in traditional medicine for hundreds of years, are a recognized source of different TRPV1 agonists, but no antagonist has yet been reported. In a search for painkiller leads, we noted for the first time a TRPV1 antagonist activity in the fresh fruits of Tetradium daniellii (Benn.) T. G. Hartley (syn. Evodia hupehensis Dode). Through a combination of extraction and purification methods with functional TRPV1-specific Ca²⁺ uptake assays (bioactivity-guided fractionation/isolation/purification); we isolated a new painkiller candidate that is a distant structural homolog of capsiate exovanilloids and endovanilloids such as anandamide, but a putative competitive inhibitor of the TRPV1. Four addnl. inactive compounds (N-isobutyl-4,5-epoxy-2E-decadienamide, geranylpsoralen, 8-(7′,8′-epoxygeranyloxy)psoralen, and xanthotoxol) were also co-purified with pellitorine. Their structures were established by extensive 1D- and 2D-NMR spectroscopic anal.¹H- and ¹³C NMR determination of the chem. structure revealed it to be pellitorine, (2E,4E)-N-(2-methylpropyl)deca-2,4-dienamide, which can compete structurally with algesics released in inflammation. In contrast to previous isolates from Evodia species, pellitorine blocked capsaicin-evoked Ca²⁺ uptake with an IC₅₀ of 154 μg/mL (0.69 mM/l). N-Isobutyl-4,5-epoxy-2E-decadienamide and geranylpsoralen, 8-(7′,8′-epoxygeranyloxy)psoralen, and xanthotoxol did not affect the TRPV1. This is the first evidence that pellitorine, an aliphatic alkylamide analog of capsaicin, can serve as an antagonist of the TRPV1 and may inhibit exovanilloid-induced pain. This study involved multiple reactions and reactants, such as (2E,4E)-N-Isobutyldeca-2,4-dienamide (cas: 18836-52-7Recommanded Product: (2E,4E)-N-Isobutyldeca-2,4-dienamide).

(2E,4E)-N-Isobutyldeca-2,4-dienamide (cas: 18836-52-7) belongs to amides. The solubilities of amides and esters are roughly comparable. Typically amides are less soluble than comparable amines and carboxylic acids since these compounds can both donate and accept hydrogen bonds. Tertiary amides, with the important exception of N,N-dimethylformamide, exhibit low solubility in water. 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.Recommanded Product: (2E,4E)-N-Isobutyldeca-2,4-dienamide

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

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

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

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Amide – Wikipedia,
Amide – an overview | ScienceDirect Topics