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编 号：F029349
分子式：C4H8O2
分子量：88.11
分子式：C4H8O2
分子量：88.11
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CAS No: 107-92-6
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生物活性：
Butyric acid is a histone deacetylase (HDAC) inhibitor, with anti-tumor effects in several cancers.
体内研究：
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. 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.
体外研究：
Butyric acid is a HDAC inhibitor. 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. 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.
Butyric acid is a histone deacetylase (HDAC) inhibitor, with anti-tumor effects in several cancers.
体内研究：
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. 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.
体外研究：
Butyric acid is a HDAC inhibitor. 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. 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.
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