Ethyl ferulate
Ethyl ferulate has anti-inflammatory property, can reduce HIV replication, it shows inhibitive effect on platelet congregation induced by ADP. It also is a potent inducer of HO-1 for the protection of brain cells against oxidative and neurodegenerative conditions.
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Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to
24 months(2-8C).
Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.
Need more advice on solubility, usage and handling? Please email to: service@chemfaces.com
The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.
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Molecules. 2014 Jun 17;19(6):8124-39.
Ethyl ferulate, a component with anti-inflammatory properties for emulsion-based creams.[Pubmed:
24941338]
Ethyl ferulate (FAEE) has been widely studied due to its beneficial heath properties and, when incorporated in creams, shows a high sun protection capacity.
METHODS AND RESULTS:
Here we aimed to compare Ethyl ferulate and its precursor, ferulic acid (FA), as free radical scavengers, inhibitors of oxidants produced by leukocytes and the alterations in rheological properties when incorporated in emulsion based creams. The cell-free antiradical capacity of Ethyl ferulate was decreased compared to FA. However, Ethyl ferulate was more effective regarding the scavenging of reactive oxygen species produced by activated leukocytes. Stress and frequency sweep tests showed that the formulations are more elastic than viscous. The viscoelastic features of the formulations were confirmed in the creep and recovery assay and showed that the Ethyl ferulate formulation was less susceptive to deformation. Liberation experiments showed that the rate of Ethyl ferulate release from the emulsion was slower compared to FA.
CONCLUSIONS:
In conclusion,Ethyl ferulate is more effective than FA as a potential inhibitor of oxidative damage produced by oxidants generated by leukocytes. The rheological alterations caused by the addition of Ethyl ferulate are indicative of lower spreadability, which could be useful for formulations used in restricted areas of the skin.
Journal of the Fourth Military Medical University, 2002,23(6):537-9.
Inhibitive effect and mechanism of Ethyl ferulate on platelet congregation induced by ADP.[Reference:
WebLink]
To investigate the inhibitory actions of Ethyl ferulate on platelet congregate induced by ADP, and the effect of platelet intracellular calcium oscillations.
METHODS AND RESULTS:
To observe platelet congregate rate induced by congregater TYXN-91. 200 mL·L~(-1) polyethylene glycol 400 as contral. Platelet intracellular calcium oscillation were observed by laser scanning Ethyl ferulate Inhibitions rate were (%) 26.3 ± 3.3, 33.4 ± 2.4, 73.4 ± 3.1 and 94.9 ± 2.7, (n = 8) at different concentration (0.1, 0.5, 1.5 and 3.0 mmol·L~(-1)), significantly increased than that of the group of ferulic acid, the change of ΔFI 4.6 ± 1.7 is much lower than resting level 10.3 ± 2.6(n = 8, P < 0.01).
CONCLUSIONS:
The inhibitive effect of Ethyl ferulate on platelet congregation induced by ADP was much more than that of ferulic acid.
Antioxid Redox Signal. 2004 Oct;6(5):811-8.
Ethyl ferulate, a lipophilic polyphenol, induces HO-1 and protects rat neurons against oxidative stress.[Pubmed:
15345140]
Ethyl ferulate (ethyl 4-hydroxy-3-methoxycinnamate) (EFE), the naturally occurring ester of ferulic acid, was able to induce HO-1 protein expression.
METHODS AND RESULTS:
Maximal expression of HO-1 mRNA and protein and a significant increase in HO activity were detected after 6 h of incubation with 15 microM EFE in astrocytes and 5 microM EFE in neurons. Higher concentrations of EFE (50 microM) caused a substantial cytotoxic effect with no change in HO-1 protein expression and activity. Exposure of astrocytes to resveratrol, a phytoalexin derived from grapes, resulted in an increase of HO-1 mRNA, but it was not able to induce HO-1 protein expression and activity. Interestingly, preincubation (12 h) of neurons with EFE resulted in an enhanced cellular resistance to glucose oxidase-mediated oxidative damage; this cytoprotective effect was considerably attenuated by zinc protoporphyrin IX, an inhibitor of HO activity.
CONCLUSIONS:
This study identifies a novel natural compound that could be used for therapeutic purposes as a potent inducer of HO-1 for the protection of brain cells against oxidative and neurodegenerative conditions.
FEBS Lett. 1997 Nov 24;418(1-2):15-8.
Protective effects of the lipophilic redox conjugate tocopheryl succinyl-ethyl ferulate on HIV replication.[Pubmed:
9414085]
Previously, we demonstrated that ferulate ethyl and tocopherol reduced HIV replication.
METHODS AND RESULTS:
In this study, we investigate whether the conjugation of both compounds (O-tocopheryl succinyl O-Ethyl ferulate) can increase HIV inhibition. We show here for the first time that O-tocopheryl succinyl O-Ethyl ferulate inhibits 80% of HIV replication (HIV-1 acute infection and HIV transmission), inhibits cell lipoperoxidation and prevents cellular glutathione consumption. Compared to ferulate ethyl and tocopheryl succinyl, O-tocopheryl succinyl O-Ethyl ferulate inhibits more HIV replication.
CONCLUSIONS:
This may be due in part to the great increase in the lipophilicity of this compound.
