Sodium ferulate

Catalog No.S4740 Synonyms: Ferulic acid sodium salt

For research use only.

Sodium ferulate (SF, Ferulic acid sodium salt), the sodium salt of ferulic acid, is a drug used in traditional Chinese medicine for treatment of cardiovascular and cerebrovascular diseases and to prevent thrombosis.

Sodium ferulate Chemical Structure

CAS No. 24276-84-4

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Biological Activity

Description Sodium ferulate (SF, Ferulic acid sodium salt), the sodium salt of ferulic acid, is a drug used in traditional Chinese medicine for treatment of cardiovascular and cerebrovascular diseases and to prevent thrombosis.
In vitro

SF is stable, water soluble. In vitro, SF (0.4 mg/mL) inhibits platelet aggregation induced by adenosine diphosphate (ADP) or collagen. At 1 mg/mL SF inhibits thrombin-induced platelet aggregation and release of [3H]5-HT from labelled platelets. The mechanism of SF action appears to be mediated by inhibition of cyclooxygenase and TXA2 synthase. In vitro SF inhibits lipid peroxide malondialdehyde (MDA) production from the platelets of rats, inhibits haemolysis induced by MDA and hydroxyl radical (OH·), and in erythrocyte membranes it inhibits lipid peroxidation induced by hydrogen peroxide (H2O2) and superoxide anions (O2-). SF is a direct scavenger of oxygen free radicals. SF is found to act as a novel non-peptide endothelin antagonist and to prevent the binding of ET-1 to its receptor[1].

In vivo SF has antithrombotic, platelet aggregation inhibitory and antioxidant activities in animals and humans. In ethanol, carbon tetrachloride-, paracetamol-, or prednisolone-induced liver toxicity in mice, SF, 0.1 g/kg intragastrically, daily for 10 days inhibits the rise of liver lipid peroxides MDA content and alleviates liver lesions by stabilizing glutathione (GSH) and related enzymes levels. In glycerol-induced renal oxidative injury in mice, SF at 0.2 g/kg i.p., reverses the increase of renal MDA content and the decrease of GSH content, glutathione peroxidase (GSH-Px), glutathione S-transferase (GST), catalase (Cat), and SOD activities induced by glycerol injection, and improves renal histology. SF has a clear protective effect in experimental myocardial ischemia. In rabbits SF reduces the area of experimental myocardial infarction by 41% and decreases the oxygen consumption of guinea pig myocardial homogenates. SF has also a protective effect in myocardial ischemia reperfusion injury of rats. Furthermore, SF has an anti-atherogenetic effect in animal models. The antiarrhythmic effects of SF have been demonstrated in experimental animal models of arrhythmia, but not yet in clinical studies. The elimination half-life of SF is about 9.86 min. The acute oral LD50 of SF in mice is 3.2 g/kg[1].

Protocol (from reference)

Cell Research:[2]
  • Cell lines: Cultured vascular smooth muscle cells (VSMCs)
  • Concentrations: 0, 50, 100 and 200 µmol/L
  • Incubation Time: 1 h
  • Method: 8,000 cells are seeded in each well of 96-well plate. After synchronous growth in DMEM including 0.5% FBS for 24 hours, VSMCs are pre-incubated in a variety of concentrations of sodium ferulate (0, 50, 100 and 200 µmol/L) for 1 hour and then stimulated with Ang Ⅱ (1 µmol/L) for another 48 hours. Following addition with CCK-8 reagent, OD values are measured at 450 nm using microplate spectrophotometer.
Animal Research:[2]
  • Animal Models: Sprague-Dawley rats(Balloon injury model)
  • Dosages: 200 mg/kg
  • Administration: by gavage

Solubility (25°C)

In vitro

Water 43 mg/mL
(198.91 mM)
DMSO 2 mg/mL
(9.25 mM)
Ethanol Insoluble

Chemical Information

Molecular Weight 216.17
Formula

C10H9O4.Na

CAS No. 24276-84-4
Storage 3 years -20°C powder
2 years -80°C in solvent
Smiles COC1=C(C=CC(=C1)C=CC(=O)[O-])O.[Na+]

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