Abstract
Ferulic acid ethyl ester (FAEE) is an ester derivative of ferulic acid and the latter is known for its anti‐inflammatory and antioxidant properties. Previous studies have shown that ferulic acid protects synaptosomal membrane system and neuronal cell culture systems against hydroxyl and peroxyl radical oxidation. FAEE is lipophilic and is able to easily penetrate into lipid bilayer. Therefore, the present study was designed to investigate the anti‐inflammatory effects of FAEE and its underlying mechanism in RAW264.7 cells. FAEE attenuated the release of NO, PGE2 and pro‐inflammatory cytokines such as IL‐1β, IL‐6 and TNF‐α in a dose‐dependent manner. Consistent with NO and PGE2 inhibition, FAEE suppressed LPS‐induced iNOS and COX‐2 expression as well as the promoter activities of COX‐2 and iNOS. In addition, FAEE pre‐treatment ameliorated ROS and superoxide anion levels in a time‐dependent manner. FAEE also dose‐dependently diminished LPS‐induced the activation mitogen‐activated protein kinases (MAPK) including JNK, ERK and p‐38 by phosphorylation. Furthermore, FAEE pre‐treatment suppressed the activation and translocation into the nucleus of NF‐κB in a dose‐dependent manner by western blotting and confocal microscopic abservation<a name=“_GoBack”></a>. The overall results indicate that FAEE may attenuate the inflammatory response of LPS‐induced RAW264.7 cells through ROS‐related MAPK/NF‐κB signaling pathway.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
