Sodium butyrate

For research use only.

Catalog No.S1999 Synonyms: NaB, Butanoic acid sodium salt

16 publications

Sodium butyrate Chemical Structure

CAS No. 156-54-7

Sodium butyrate (NaB, Butanoic acid sodium salt), sodium salt of butyric acid, is a histone deacetylase inhibitor and competitively binds to the zinc sites of class I and II histone deacetylases (HDACs). Sodium butyrate (NaB) inhibits cell cycle progression, promotes differentiation, and induces apoptosis and autophagy in several types of cancer cells.

Selleck's Sodium butyrate has been cited by 16 publications

2 Customer Reviews

  • U87 cells were cultured with DMSO or 10 µM 5azadC for 72 h. For the latter, 1 µM Trichostatin A (TSA), 10 mM sodium butyrate (NaBu), 5 mM nicotinamide (NAM), or 0.5 µM apicidin were added in the last 24 h. IFNLR1 expression was determined by RT-qPCR.

    PLoS Biol 2014 12(1), e1001758. Sodium butyrate purchased from Selleck.

  • Effects of combination of either MS-275, apicidin, SAHA or sodium butyrate (NaB) with bortezomib on proliferation of Wp-restricted BL cells. P3HR1-c16 cells were treated with combination of NaB (0, 0.6, 1.2, 2.4, 4.8 and 9.6 mM) for 48 h. Cell proliferation was determined by MTT assay and presented as percentages of cell proliferation of treated cells compared with those of untreated cells. Synergisms of proliferation inhibition of the cells following treatment with different drug combinations were analysed by isobologram analysis.

    Br J Haematol 2014 167(5), 639-50. Sodium butyrate purchased from Selleck.

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Biological Activity

Description Sodium butyrate (NaB, Butanoic acid sodium salt), sodium salt of butyric acid, is a histone deacetylase inhibitor and competitively binds to the zinc sites of class I and II histone deacetylases (HDACs). Sodium butyrate (NaB) inhibits cell cycle progression, promotes differentiation, and induces apoptosis and autophagy in several types of cancer cells.
Targets
Histone deacetylase [6]
()
In vitro

Butyrate mediates growth inhibition of colonic cancer cells and thereby to elucidate the molecular link between a high-fiber diet and the arrest of colon carcinogenesis. Butyrate induces p21 mRNA expression in an immediate-early fashion, through transactivation of a promoter cis-element(s) located within 1.4 kb of the transcriptional start site, independent of p53 binding. [1] Sodium butyrate, at physiological concentrations, induces apoptosis in 2 adenoma cell lines, RG/C2 and AA/Cl, and in the carcinoma cell line PC/JW/FI. [2] Butyrate exerts potent effects on a variety of colonic mucosal functions such as inhibition of inflammation and carcinogenesis, reinforcing various components of the colonic defence barrier and decreasing oxidative stress. [3] Butyrate inhibits most HDAC except class III HDAC and class II HDAC6 and -10. Butyrate also is the most effective fatty acid in stimulating or repressing the expression of specific genes. [4]
Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
human K562 cells NUK4[|Z2WHKxbHnm[ZJifGmxbjDhd5NigQ>? NEXMfXkyKG2P M2Xy[WFvfGmycn;sbYZmemG2aY\lJIFkfGm4aYT5JIFo[Wmwc4SgbJVu[W5iS{W2NkBk\WyuczDheEAyKG2PIHnuJJBz\XOnbnPlJI9nKGe3YX7vd4lv\Q>? MW[yN|k{Pzl5OR?=
human H1299 cells NFnhRWZHfW6ldHnvckBie3OjeR?= MXG3JIRigXN? NGS0PW5KdmirYnn0bY9vKG:oIHj1cYFvKFWVUEGvWWFHOSCrbjDoeY1idiCKMUK5PUBk\WyuczDhd5Nme3OnZDDhd{Bz\WS3Y4Tpc44hcW5iY3;sc456KG[xcn3heIlwdiCjZoTldkA4KGSjeYOsJGVEPTB;MzFOwG0> Mn7nNlUzOjl4NEO=
human JEG3 cells Mkj4SpVv[3Srb36gZZN{[Xl? M3zxe2lvcGmkaYTpc44hd2ZiYYLvcYF1[XOnIHnuJIh2dWGwIFrFS|Mh[2WubIOgZpkhe2OrboTpcIxifGmxbjDzdIVkfHKxbXX0dpktKEmFNUC9NE4xODF3IN88US=> NFnGPWIzODF2OEW2OC=>

... Click to View More Cell Line Experimental Data
Assay
Methods Test Index PMID
Western blot
Cyclin D3 / CDK4 / CDK6 / CDK2 ; 

PubMed: 24280698     


Proliferating VSMC were treated with different concentration of butyrate or TSA for 48 h to determine dose- and time-dependent effects of butyrate and TSA on G1-specific cell cycle proteins. At the end of treatment, cell lysates were prepared and processed for western analysis of cyclin D3, cdk4, cdk6, cdk2. Immunoblotting of ERK1/2 was performed with the same lysate to normalize the protein loading.

p15INK4b / p21Cip1 ; 

PubMed: 24280698     


Proliferating VSMC were treated with different concentration of butyrate or TSA for 48 h to determine dose- and time-dependent effects of butyrate and TSA on G1-specific cell cycle proteins. At the end of treatment, cell lysates were prepared and processed for western analysis of p15INK4b and p21Cip1.

Phospho-H3 Ser10 / Acetyl-H3Lys9 / Acetyl-H3Lys14 / Dimethyl-H3 ; 

PubMed: 24280698     


Proliferating VSMC were treated with different concentration of butyrate or TSA for 48 h (A) or treated with 5 mM butyrate or 0.5 µM TSA for indicated periods of time (B); to determine dose- and time-dependent effects of butyrate and TSA on indicated site-specific modifications of histone H3, respectively. At the conclusion of the treatment, VSMC were processed for western analysis using appropriate antibodies to assess the effects of butyrate and TSA on histone H3 modifications. ERK1/2 was immunoblotted and used as loading control. The results shown are representative of three independent experiments. The density of each band is measured and normalized to protein loading. The data obtained are analyzed and expressed as mean ± S.D. Phospho-H3Serine10, acetyl-H3Lys9, acetyl-H3Lys14, di-methyl-H3Lys9 and di-methyl-H3Lys4 modifications stimulated by butyrate vs. control are significant to very significant (p < 0.01 to p < 0.001) depending on the concentrations of butyrate except for di-methyl-H3Lys4 modification, which is not significant at 0.5 and 1 mM butyrate concentration (A). Changes induced by TSA vs. DMSO are significant to very significant (p < 0.01 to p < 0.001) with the exception of acetyl-H3Lys14 and di-methyl-H3Lys4 at 0.1 µM TSA (A). Time-dependent changes in levels of phospho-H3Serine10, acetyl-H3Lys9, acetyl-H3Lys14, di-methyl-H3Lys9 and di-methyl-H3Lys4 histone H3 modifications are significant to very significant (p < 0.05 to p < 0.001) both in butyrate and TSA treated VSMC compared to untreated control at all periods of time with the exception of di-methyl-H3Lys9 at 6 h (B).

24280698
Immunofluorescence
Acetyl-H3Lys9; 

PubMed: 24280698     


Effect of butyrate and TSA on acetylation of H3Lys9, and H3Lys14 was also determined by intracellular immunofluorescence staining of H3Lys9, and H3Lys14 followed by nuclear staining with Hoechst. VSMC treated with butyrate or TSA for 24 h were immunostained with respective antibodies and images of immunostained VSMC were captured using Nikon fluorescence microscope with a CCD camera (400× magnification).

24280698
In vivo Sodium butyrate significantly extends survival in a dose-dependent manner, improves body weight and motor performance, and delays the neuropathological sequelae in the R6/2 transgenic mouse model of Huntington's disease (HD). Sodium butyrate also increases histone and specificity protein-1 acetylation and protects against 3-nitropropionic acid neurotoxicity. [5]

Protocol

Solubility (25°C)

In vitro Water 22 mg/mL (199.83 mM)
DMSO Insoluble
Ethanol '22 mg/mL

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Chemical Information

Molecular Weight 110.09
Formula

C4H7NaO2
CAS No. 156-54-7
Storage powder
in solvent
Synonyms NaB, Butanoic acid sodium salt
Smiles CCCC(=O)[O-].[Na+]

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Clinical Trial Information

NCT Number Recruitment interventions Conditions Sponsor/Collaborators Start Date Phases
NCT00800930 Completed Biological: Sodium Butyrate|Biological: Saline Shigellosis International Centre for Diarrhoeal Disease Research Bangladesh|Swedish International Development Cooperation Agency (SIDA)|Karolinska Institutet January 2005 Phase 2

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HDAC Signaling Pathway Map

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID