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Overview
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Background
Sodium butyrate is a kind of histone deacetylases (HDACs) inhibitors studied clinically, which works on histones and transcription factors to modulate transcription [1].
Interaction of HDACs and histone acetyltransferases determines histone acetylation, which affects the final transcription process. The transcription dysregulation results in functional and degenerative changes [2].
In the adenoma RG/C2 cell line, sodium butyrate reduced the number of attached cells to 50% of that of the control group, and the number of floating cells is increased induced by cell apoptosis. Compare with RG/C2, AA/CI showed more sensitivity to sodium butyrate [3].
In the experiments of the R6/2 cell line transgenic Huntingtin disease (HD) mouse model, seven different intraperitoneal dosings of sodium butyrate were administrated daily. The survival time, weight and athletic ability were improved together, and the neuropathologic sequelae were delayed, too. Besides, sodium butyrate increased the acetylation level of histone and specificity protein-1 and prevent the neurotoxicity inducing by 3-nitropropionic acid [1].[1]. Ferrante R J, Kubilus J K, Lee J, et al. Histone deacetylase inhibition by sodium butyrate chemotherapy ameliorates the neurodegenerative phenotype in Huntington's disease mice [J]. Journal of Neuroscience, 2003, 23(28): 9418-9427.
[2]. Cha J H. Transcriptional dysregulation in Huntington's disease [J]. Trends in Neurosciences, 2000, 23(9): 387-392.
[3]. Hague A, Manning A M, Hanlon K A, et al. Sodium butyrate induces apoptosis in human colonic tumour cell lines in a p53-independent pathway: implications for the possible role of dietary fibre in the prevention of large-bowel cancer [J]. International Journal of Cancer, 1993, 55(3): 498-505.
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