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Niacin

Manufactured by Merck Group
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Niacin is a laboratory-grade chemical compound that serves as a versatile raw material for various applications. It is a water-soluble vitamin, also known as vitamin B3, which plays a crucial role in energy metabolism and various physiological processes. Niacin is commonly used in the production of pharmaceuticals, dietary supplements, and as a food additive. Its core function is to provide an essential nutrient for the maintenance of normal bodily functions.

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Lab products found in correlation

Riboflavin, by Merck Group (8 mentions) Pantothenic acid, by Merck Group (5 mentions) Thiamine, by Merck Group (4 mentions) Ascorbic acid, by Merck Group (4 mentions) Formic acid, by Merck Group (3 mentions) Pyridoxine, by Merck Group (3 mentions) Thiamin, by Merck Group (3 mentions) Biotin, by Merck Group (3 mentions) Thiamine hydrochloride, by Merck Group (3 mentions) Folic acid, by Merck Group (3 mentions) Acetonitrile, by Thermo Fisher Scientific (3 mentions) Methanol, by Thermo Fisher Scientific (3 mentions) Sodium hydroxide (naoh), by Merck Group (3 mentions) Sodium chloride (nacl), by Merck Group (3 mentions) Formic acid, by Thermo Fisher Scientific (3 mentions) Nicotinamide, by Merck Group (2 mentions) Lipopolysaccharides (lps), by Merck Group (2 mentions) Caffeine, by Merck Group (2 mentions) C18 silica column, by Merck Group (2 mentions) Gallium 3 nitrate, by Merck Group (2 mentions)

45 protocols using niacin

1

Niacin Receptor Expression and Heat Stress Response

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Experiment 1: Distribution of niacin Receptor in Bovine Tissues and Cells. To identify the expression of niacin receptor GPR109A in bovine tissues and cells, reverse-transcription PCR was performed on RNA samples from the tissues of 3 cows (liver, uterus, ovary, skin, and udder), and from 3 types of cells (BEND, MAC-T, and BMEC). Expression levels of GPR109A were compared among tissues using qPCR.
Experiment 2: Effects of niacin Treatment on Heat Shock Responses of Bovine Cells. All 3 cell types were subjected to niacin (Sigma-Aldrich) treatment at 0 or 0.01 mM (1.23 μg/mL), and exposed to thermoneutral conditions (37°C) or heat stress (42°C) for 8 h. The dose of niacin used matched niacin levels in the plasma of cows (Rungruang et al., 2014) . Cells were cultured in 24-well plates. Two wells of cells were pooled for 1 sample, and 3 samples stood for each dose and environment. The mRNA expression of heat shock proteins (HSP70 and HSP27) and prostaglandin E synthesis-related enzymes (COX-1, COX-2, mPGES-1 and mPGES-2) were evaluated in MAC-T, BMEC, and BEND. The C t values of the genes of interest were normalized with those of reference gene RPS9.
Xiao Y., Rungruang S., Hall L.W., Collier J.L., Dunshea F.R, & Collier R.J. (2017). Effects of niacin and betaine on bovine mammary and uterine cells exposed to thermal shock in vitro. Journal of dairy science, 100(5).
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2

Biosynthesis and Purification of Yersiniabactin

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Ybt was generated from UTI89ΔentB grown in M63 minimal salts medium supplemented with 0.2% glycerol (v/v) and 10mg ml-1 niacin (Sigma) as previously described 53 . [13C6]Ybt with a 13C-substituted phenolic ring was produced from UTI89ΔentB ΔybtS grown in M63 minimal salts medium supplemented with 0.2% glycerol (v/v), 13C6-labeled salicylic acid and 10mg ml-1 niacin (Sigma).[13C21]Ybt was produced by UTI89Δfur in media supplemented with [13C3]glycerol as previously described 53 . Metal-Ybt complexes were produced by adding iron(III) chloride, copper(II) sulfide or gallium(III) nitrate (Sigma) to Ybt. Metal-Ybt was applied to a methanol conditioned C18 silica column (Sigma) and eluted with 80% methanol as previously described 56 . Eluates were concentrated by lyophilization. Dried samples were resuspended in deionized water and purified through high-performance liquid chromatography (HPLC) using a C18 silica column (Whatman Partisil). Metal-Ybt containing fractions were collected, dried down using a lyophilizer and resuspended in deionized water. Metal-Ybt concentrations were determined using previously described extinction coefficients 56 .
Koh E.I., Robinson A.E., Bandara N., Rogers B.E, & Henderson J.P. (2017). Copper import in Escherichia coli by the yersiniabactin metallophore system. Nature chemical biology, 13(9), 1016-1021.
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3

Modulating Co-culture Metabolism with Niacin and ES2

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Co-cultures were treated using nicotinic acid (niacin, #PHR1276, Sigma-Aldrich) diluted in MEM (#11090081, ThermoFisher Scientific) at a final concentration of 5 mM. Endosidin-2 (ES2; #SML168, 5 mg, Sigma-Aldrich) was diluted in MEM at a final concentration of 1 µM. niacin or ES2 were added concomitantly to ascorbic acid at Day 6 of the co-culture.
El-Bazzal L., Ghata A., Estève C., Gadacha J., Quintana P., Castro C., Roeckel-Trévisiol N., Lembo F., Lenfant N., Mégarbané A., Borg J.P., Lévy N., Bartoli M., Poitelon Y., Roubertoux P.L., Delague V, & Bernard-Marissal N. (2022). Imbalance of NRG1-ERBB2/3 signalling underlies altered myelination in Charcot–Marie–Tooth disease 4H. Brain, 146(5), 1844-1858.
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4

Hyperglycemia Effects on Human Retinal Endothelial Cells

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Human retinal endothelial cells (HREC) were purchased from ScienCell Research Laboratories (America). All cells were grown in Endothelial Cell Medium (ECM) (ScienCell, America). Cells were treated for 72 h with ECM containing of the following: 5 mM D-glucose (euglycemic control)(CON group); 25 mM D-glucose (hyperglycemia) (HI group); 25 mM D-glucose (hyperglycemia + Niacin (1 mM, Sigma Chemical Co., USA) (NA group); 25 mM D-glucose (hyperglycemia) + Niacin (1 mM) + microRNA126 inhibitor (NI group). HREC cells were treated miR-126 inhibitor (miR-126-inhibitor) (Invitrogen, CA, USA) using Lipofectamine 2000.
Wang Y, & Yan H. (2016). MicroRNA-126 contributes to Niaspan treatment induced vascular restoration after diabetic retinopathy. Scientific Reports, 6, 26909.
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5

Biosynthesis and Purification of Yersiniabactin

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Ybt was generated from UTI89ΔentB grown in M63 minimal salts medium supplemented with 0.2% glycerol (v/v) and 10mg ml-1 niacin (Sigma) as previously described 53 . [13C6]Ybt with a 13C-substituted phenolic ring was produced from UTI89ΔentB ΔybtS grown in M63 minimal salts medium supplemented with 0.2% glycerol (v/v), 13C6-labeled salicylic acid and 10mg ml-1 niacin (Sigma).[13C21]Ybt was produced by UTI89Δfur in media supplemented with [13C3]glycerol as previously described 53 . Metal-Ybt complexes were produced by adding iron(III) chloride, copper(II) sulfide or gallium(III) nitrate (Sigma) to Ybt. Metal-Ybt was applied to a methanol conditioned C18 silica column (Sigma) and eluted with 80% methanol as previously described 56 . Eluates were concentrated by lyophilization. Dried samples were resuspended in deionized water and purified through high-performance liquid chromatography (HPLC) using a C18 silica column (Whatman Partisil). Metal-Ybt containing fractions were collected, dried down using a lyophilizer and resuspended in deionized water. Metal-Ybt concentrations were determined using previously described extinction coefficients 56 .
Koh E.I., Robinson A.E., Bandara N., Rogers B.E, & Henderson J.P. (2017). Copper import in Escherichia coli by the yersiniabactin metallophore system. Nature chemical biology, 13(9), 1016-1021.
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6

Niacin-induced TRPV1 Activation in Mice

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Wild-type C57BL/6 mice were obtained from Charles River Laboratories (Wilmington, MA). TRPV1–/– (KO) mice were obtained from Jackson Laboratories (Sacramento, CA). All mice were adult males (3–6 months of age). For the experiments, mice were anesthetized using pentobarbital (Sigma-Aldrich, St. Louis, MO) at a dose of 60 mg/kg dissolved in 10% ethanol given by intraperitoneal (IP) injection. Niacin (Sigma-Aldrich) was administered by IP injection at a dose of 30 mg/kg dissolved in 0.9% saline (15 mg/mL). The TRPV1 antagonist AMG9810 [(E)-3-(4-t-Butylphenyl)-N-(2,3-dihydrobenzo[b][1,4] dioxin-6-yl)acrylamide] (Sigma-Aldrich) was administered by IP injection at doses of 20 and 40 mg/kg in PEG400 (20 mg/mL). The TRPV1 agonist capsaicin (Sigma-Aldrich) was administered topically at a dose of 0.2 mg in acetone (20 mg/mL).
Clifton H.L., Inceoglu B., Linlin M., Zheng J, & Schaefer S. (2015). TRPV1 Channels Are Involved in Niacin-induced Cutaneous Vasodilation in Mice. Journal of cardiovascular pharmacology, 65(2), 184-191.
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7

Curcumin Nicotinate Modulates Cell Death

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Mouse monoclonal anti-β-actin, rabbit polyclonal anti-bcl-2, rabbit polyclonal anti-Puma, rabbit polyclonal anti-cleaved-Bid, rabbit polyclonal anti-Bak, rabbit polyclonal anti-cleaved PARP, rabbit polyclonal anti-p53 and rabbit polyclonal anti-P21 antibodies were purchased from Cell Signaling Technology (Danvers, MA, USA). Horseradish peroxidase linked secondary sheep anti-mouse and rabbit anti-horse IgG were obtained from GE Healthcare (Chicago, IL, USA). Propidium iodide (PI) and Annexin V were purchased from BD Pharmingen (Franklin Lakes, NJ, USA). Complete lysis-M was purchased from Roche Applied Science (Indianapolis, IN, USA). AO/EB nuclear dyes were purchased from Beyotime (Shanghai, China). Curcumin, niacin, 3-[4–dimethylthiazol-2-yl]-2, 5-diphenyltetrazoliumbromide (MTT) and other chemicals were purchased from Sigma-Aldrich (St Louis, MO, USA). Curcumin nicotinate (CN) was in-home synthesized. For experimental uses, CN was dissolved in DMSO at 10 mM as stock solution and then diluted to concentrations indicated.
He Y.C., He L., Khoshaba R., Lu F.G., Cai C., Zhou F.L., Liao D.F, & Cao D. (2019). Curcumin Nicotinate Selectively Induces Cancer Cell Apoptosis and Cycle Arrest through a P53-Mediated Mechanism. Molecules, 24(22), 4179.
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8

AngII Infusion and Niacin/Nicotinamide Treatment in LDLR KO Mice

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AngII (Enzo Life Sciences, 1000 ng/kg/min) was infused into male LDLR KO mice via osmotic mini-pumps (ALZET Model 2004) as described.20 (link) Mice were treated with oral niacin (0.3% wt/vol) or nicotinamide (0.1% or 0.4% wt/vol, purchased from Sigma-Aldrich)8 (link),19 (link),23 (link),24 (link) supplemented in drinking water for 2 days prior to mini-pump implantation and continued throughout the study. In some experiments, mice were co-treated with 6-chloro-2,3,4,9-tetrahydro-1H-carbazole-1-carboxamide (EX-527, 20 mg/kg body weight) to inhibit Sirt1 activity.25 Blood pressure measurements were obtained using a validated tail-cuff method (Coda 6, Kent Scientific).18 (link) Serum cholesterol and triglyceride were quantified using commercial assays (Wako Pure Chemical Industries). Two to four weeks after mini-pump implantation, mice were euthanized, aortic outer diameter was measured, and tissues were collected for analysis.
Horimatsu T., Blomkalns A.L., Ogbi M., Moses M., Kim D., Patel S., Gilreath N., Reid L., Benson T.W., Pye J., Ahmadieh S., Thompson A., Robbins N., Mann A., Edgell A., Benjamin S., Stansfield B.K., Huo Y., Fulton D.J., Agarwal G., Singh N., Offermanns S., Weintraub N.L, & Kim H.W. (2019). Niacin protects against abdominal aortic aneurysm formation via GPR109A independent mechanisms: role of NAD+/nicotinamide. Cardiovascular Research, 116(14), 2226-2238.
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9

Macrophage GPR109A and NF-κB Regulation

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BALB/c murine macrophage RAW264.7 cells were a gift from Dr. Krishnan Dhandapani, Augusta University. This murine macrophage cell line was chosen for this study because of its high expression of GPR109A and large availability compared to human macrophage cell lines which are SV40 T antigen modified; the genetic modification of human macrophages by SV40 T antigen may alter their morphology. Cells were cultured in RPMI medium 1640 (Life Technologies, Rockville, MD, USA), supplemented with 10% heat inactivated fetal bovine serum (FBS), 2 mM glutamine, and penicillin/streptomycin cocktail and incubated in a humidified incubator with 5% CO2 at 37 °C. Cells were treated with 400 μM niacin (Sigma-Aldrich, St. Louis, MO, USA) overnight followed by stimulation with LPS (20 ng/mL) for 20 min at 37 °C, 5% CO2. The expression of cytokine mRNA was determined by real time polymerase chain reactions (RT-PCR) and the expression of GPR109A, p-NF-κB, Histone 3 (H3), Rho-GDI alpha (ρGDi-α) and β-actin was confirmed using respective antibodies in Western blot assays.
Giri B., Belanger K., Seamon M., Bradley E., Purohit S., Chong R., Morgan J.C., Baban B, & Wakade C. (2019). Niacin Ameliorates Neuro-Inflammation in Parkinson’s Disease via GPR109A. International Journal of Molecular Sciences, 20(18), 4559.
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10

Dextran Sulfate Sodium Colitis Model

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Dextran sulfate sodium (DSS) was purchased from MP Biomedicals (LLC, Santa Ana, California, USA). TNBS, LPS, Evan's blue, and niacin were purchased from Sigma Chemical Company (Sigma‐Aldrich, St. Louis, MO, USA). PGD2 and BW245C were obtained from Cayman Chemical Company (Cayman Chemical, Ann Arbor, MI, USA). Percoll solution was from Biosharp (Biosharp, Hefei, China). IL‐13 was purchased from Peprotech (Peprotech, Rocky Hill, USA). TdT fluorescence in situ Apoptosis Detection kit was from Yeasen Biological Technology (Yeasen, Shanghai, China). Annexin V‐FITC Apoptosis Detection Assay kit was obtained from Dojindo Laboratories (Dojindo, Shanghai, China).
Li J., Kong D., Wang Q., Wu W., Tang Y., Bai T., Guo L., Wei L., Zhang Q., Yu Y., Qian Y., Zuo S., Liu G., Liu Q., Wu S., Zang Y., Zhu Q., Jia D., Wang Y., Yao W., Ji Y., Yin H., Nakamura M., Lazarus M., Breyer R.M., Wang L, & Yu Y. (2017). Niacin ameliorates ulcerative colitis via prostaglandin D2‐mediated D prostanoid receptor 1 activation. EMBO Molecular Medicine, 9(5), 571-588.
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