Butyric acid is a histone deacetylase (HDAC) inhibitor, with anti-tumor effects in several cancers.

Butyric acid is a HDAC inhibitor^[1]. Butyric acid induces morphological changes, inhibits cell proliferation and impairs cell viability in NPC cells. Sodium Butyrate (1, 5, 10 mM) is cytotoxic to NPC cells, inducing a dose- and time-dependent decrease in cell viability, in both 5-8F and 6-10B cells. Sodium Butyrate induces nasopharyngeal carcinoma cell apoptosis by activating the mitochondrial apoptotic axis. Moreover, SOCE inhibition and disruption of the CRAC channel can attenuate the apoptosis induced by Sodium Butyrate^[2]. Sodium butyrate significantly decreases cell viability, accompanied by reduced levels of p-mTOR and PCNA protein. Sodium butyrate dose-dependently induces cell cycle arrest in G0/G1 phase and reduces the numbers of cells in S phase. In addition, relative expression of p21, p27, and pro-apoptosis bak genes, and protein levels of p21Waf1/Cip1, p27Kip1, cyclinD3, CDK4, and Cleave-caspase3 are increased by higher concentrations of sodium butyrate (1, 5, 10 mM), and the levels of cyclin D1 and CDK6 are reduced by 5 and 10 mM butyrate^[4].

Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.

Sodium Butyrate (300 mg/kg, s.c.) provides almost complete neuroprotection in comparison with non-treated animals. Sodium butyrate results in an increased number of microglial cells to 150% of vehicle-treated animals in the ipsilateral side. Sodium butyrate promotes the polarization of microglia from M1- to M2-like phenotype after neonatal hypoxia-ischemia^[3]. Sodium butyrate (300 mg/kg, s.c.) in combination with AK-7 (20 mg/kg, i.p.) significantly alleviates this reduction of the time spent exploring new objects, ameliorates the reduction of the number of Ki67-positive cells and DCX-immunoreactive neuroblasts in the dentate gyrus of the mice. In addition, sodium butyrate reverses SIRT2-related age phenotypes^[5].

Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.

88.11

C₄H₈O₂

107-92-6

液体

Colorless to light yellow

丁酸

Room temperature in continental US; may vary elsewhere.

• [1]. Huang W, et al. Inhibition of store-operated Ca2+ entry counteracts the apoptosis of nasopharyngeal carcinoma cells induced by sodium butyrate. Oncol Lett. 2017 Feb;13(2):921-929.  [Content Brief]

  [2]. Jaworska J, et al. The potential neuroprotective role of a histone deacetylase inhibitor, sodium butyrate, after neonatal hypoxia-ischemia. J Neuroinflammation. 2017 Feb 10;14(1):34.  [Content Brief]

  [3]. Jung HY, et al. Sirtuin-2 inhibition affects hippocampal functions and sodium butyrate ameliorates the reduction in novel object memory, cell proliferation, and neuroblast differentiation. Lab Anim Res. 2016 Dec;32(4):224-230.  [Content Brief]

  [4]. Qiu Y, et al. Effect of sodium butyrate on cell proliferation and cell cycle in porcine intestinal epithelial (IPEC-J2) cells. In Vitro Cell Dev Biol Anim. 2017 Jan 27.  [Content Brief]

  [5]. Wang P, et al. Sodium butyrate triggers a functional elongation of microglial process via Akt-small RhoGTPase activation and HDACs inhibition. Neurobiol Dis. 2018 Mar;111:12-25.  [Content Brief]

Cells are seeded at a density of 2,000 cells/well in 96-well plates with 200 μL culture medium containing Sodium Butyrate at different concentrations. Then, the cells are consecutively cultured for 72 h. Every 24 h, 20 μL 5 mg/mL MTT solution is added into the corresponding well, and the cells are cultured for another 4 h. Then, the solution is replaced with 150 μL DMSO, followed by gentle agitation of the plates for 15 min at room temperature. Finally, the absorbance at 492 nm is measured to represent the cell viability^[2].

Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.

Rats^[3]
Seven-day-old rat pups are subjected to unilateral carotid artery ligation followed by 60 min of hypoxia (7.6% O₂). Sodium Butyrate (300 mg/kg) is administered in a 5-day regime with the first injection given immediately after hypoxic exposure. The damage of the ipsilateral hemisphere is evaluated by hematoxylin-eosin staining 6 days after the insult. Samples are collected at 24 and 48 h and 6 days^[3].

Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.

• [1]. Huang W, et al. Inhibition of store-operated Ca2+ entry counteracts the apoptosis of nasopharyngeal carcinoma cells induced by sodium butyrate. Oncol Lett. 2017 Feb;13(2):921-929.  [Content Brief]

  [2]. Jaworska J, et al. The potential neuroprotective role of a histone deacetylase inhibitor, sodium butyrate, after neonatal hypoxia-ischemia. J Neuroinflammation. 2017 Feb 10;14(1):34.  [Content Brief]

  [3]. Jung HY, et al. Sirtuin-2 inhibition affects hippocampal functions and sodium butyrate ameliorates the reduction in novel object memory, cell proliferation, and neuroblast differentiation. Lab Anim Res. 2016 Dec;32(4):224-230.  [Content Brief]

  [4]. Qiu Y, et al. Effect of sodium butyrate on cell proliferation and cell cycle in porcine intestinal epithelial (IPEC-J2) cells. In Vitro Cell Dev Biol Anim. 2017 Jan 27.  [Content Brief]

  [5]. Wang P, et al. Sodium butyrate triggers a functional elongation of microglial process via Akt-small RhoGTPase activation and HDACs inhibition. Neurobiol Dis. 2018 Mar;111:12-25.  [Content Brief]