Sodium Butyrate – cheap cancer killer.

Dr. Weeks’ Comment: sodium butyrate is a potent under-utilized anti-cancer agent. Ask your oncologists about  this potent anti-inflammatory agent.


Nephrol Dial Transplant. 2012 Jan 23. [Epub ahead of print]

Sodium butyrate decreases the activation of NF-κB reducing inflammation and oxidative damage in the kidney of rats subjected to contrast-induced nephropathy.

Machado RA, Constantino LD, Tomasi CD, Rojas HA, Vuolo FS, Vitto MF, Cesconetto PA, de Souza CT, Ritter C, Dal-Pizzol F.


Contrast-induced nephropathy (CIN) is associated with a combination of hypoxic and toxic renal tubular damage, renal endothelial dysfunction and altered intra-renal microcirculation. Recently, sodium butyrate (SB) has been focused on since it possesses anti-inflammatory activities. Thus, based on the lack of information on the effects of SB in acute kidney injury (AKI), we investigated the possible effects of SB after CIN in rats.


The current experiment suggests that NF-κB induced an inflammatory response after CIN and sodium butyrate SB could inhibit NF-κB expression protecting against CIN in rats.



PLoS One. 2012;7(1):e30143. Epub 2012 Jan 12.

c-MET Protects Breast Cancer Cells from Apoptosis Induced by Sodium Butyrate.

Sun B, Liu R, Xiao ZD, Zhu X.


State Key Laboratory of Bioelectronics, School of Biological Science and Medical Engineering, Southeast University, Nanjing, China.


Sodium Butyrate (NaBu) is regarded as a potential reagent for cancer therapy. In this study, a specific breast cancer cell population that is resistant NaBu treatment was identified. These cells possess cancer stem cell characters, such as the capability of sphere formation in vitro and high tumor incident rate (85%) in mouse model. Forty percent of the NaBu resistant cells express the cancer stem cells marker, the CD133, whereas only 10% intact cells present the CD133 antigen. Furthermore, the endogenous expressing c-MET contributes to the survival of cancer stem cell population from the treatment of NaBu. The CD133+ group also presents a higher level of c-MET. A combination treatment of MET siRNA and NaBu efficiently prohibited the breast cancer progression, and the incident rate of the tumor decrease to 18%. This study may help to develop a new and alternative strategy for breast cancer therapy.



Mol Biol Rep. 2012 Jan 7. [Epub ahead of print]

Dual effects of sodium butyrate on hepatocellular carcinoma cells.

Jiang W, Guo Q, Wu J, Guo B, Wang Y, Zhao S, Lou H, Yu X, Mei X, Wu C, Qiao S, Wu Y.


State Key Laboratory of Genetic Engineering, Institute of Genetics, Fudan University, 220 Handan Road, Shanghai, 200433, People’s Republic of China.


Sodium butyrate (NaBu), a histone deacetylase inhibitor, has been shown to inhibit cell growth, induce cell differentiation and apoptosis in multiple cell lines. In present study, we revealed the dual effects of NaBu in regulating hepatocellular carcinoma (HCC) cells. In two different HCC cell lines, SK-Hep1 and SMMC-7721, low concentrations of NaBu induced a significant increase in cell growth ratio and S-phase cell percentage, accompanied by a reduced p21 Cip1 expression at both mRNA and protein levels, while dissimilarly, high concentrations of NaBu inhibited cell growth and induced G1 arrest through up-regulation of p21 Cip1 and p27 Kip1 protein expression. The reduction of p45 Skp2 expression further indicated that the ubiquitin-mediated protein degradation might play a role in NaBu-induced up-regulation of p21 Cip1 and p27 Kip1. Moreover, the high concentration of NaBu was also able to trigger HCC cell apoptosis. Taken together, these results demonstrate the distinct effects of NaBu at different dosages. This finding may contribute to develop more effective tumor therapeutic protocols of NaBu in HCC.




Oncol Rep. 2011 Dec 8. doi: 10.3892/or.2011.1585. [Epub ahead of print]

Sodium butyrate-induced DAPK-mediated apoptosis in human gastric cancer cells.

Shin H, Lee YS, Lee YC.


Department of Internal Medicine, Institute of Gastroenterology, Yonsei University College of Medicine, Seoul, Republic of Korea.


Epigenetic mechanisms of histone acetylation/deacetylation play an important role in the regulation of gene expression associated with the cell cycle and apoptosis. Recently, sodium butyrate, a histone deacetylase (HDAC) inhibitor, has been shown to exhibit anticancer effects via differentiation and apoptosis of cancer cells. Sodium butyrate may be a potential anticancer chemotherapeutic drug; however, the precise mechanism underlying the anticancer effects of sodium butyrate has not been clearly elucidated. …. These data suggest that DAPK expression prompts apoptosis by reducing the FAK protein level in sodium butyrate-induced apoptosis of human gastric cancer cells.



Neuroscience. 2012 Jan 3;200:42-9. Epub 2011 Oct 28.

Memory impairment induced by brain iron overload is accompanied by reduced H3K9 acetylation and ameliorated by sodium butyrate.

da Silva PF, Garcia VA, Dornelles Ada S, da Silva VK, Maurmann N, Portal BC, Ferreira RD, Piazza FC, Roesler R, Schröder N.


Neurobiology and Developmental Biology Laboratory, Faculty of Biosciences, Pontifical Catholic University, 90619-900 Porto Alegre, RS, Brazil.


Iron accumulation in the brain has been associated to the pathogenesis of neurodegenerative disorders. We have previously demonstrated that iron overload in the neonatal period results in severe and persistent memory deficits in adult rats. Alterations in histone acetylation have been associated with memory deficits in models of neurological disorders. Here we examine histone acetylation in the brain and the effects of the histone deacetylase inhibitor (HDACi) sodium butyrate (NaB) on memory in the neonatal iron overload model in rats. …..A single systemic injection of NaB (1.2 g/kg) immediately after training ameliorated iron-induced memory impairments. The results suggest that a reduction in H3K9 acetylation might play a role in iron-induced memory impairment and support the view that HDACis can rescue memory dysfunction in models of brain disorders.

Copyright © 2011 IBRO. Published by Elsevier Ltd. All rights reserved.

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