Oleic acid reduces lipopolysaccharide‐induced expression of iNOS and COX‐2 through inhibition of reactive oxygen species and NF‐¥êB activation in BV2 murine microglial cells

Abstract

Microglial cells are the major cell types involved in neuroinflammation, resulting in brain tissue damages during cerebral ischemia and neurodegenerative disorders. In this study, we examined the effects of the monounsaturated fatty acid oleic acid (C18:1, OA) on LPS‐induced proinflammatory mediators and the mechanisms involved in BV2 microglial cells. OA inhibited LPS‐induced the expression of iNOS and COX‐2 mRNA and proteins as well as the production of NO and prostaglandins. We showed that OA inhibited LPS‐induced NF‐κB activation and phosphorylation of inhibitor κB kinase (IKK). We also showed that OA inhibited LPS‐induced phosphorylation of Akt and p38 and PI 3‐kinase activation, but not that of ERK. Finally, we showed that OA reduced the reactive oxygen species (ROS) accumulation and an antioxidant N‐acetylcysteine inhibited NF‐κB activation and IKK phosphorylation in LPS‐stimulated BV2 cells. Taken together, our results suggest that OA has an anti‐inflammatory effect by inhibiting ROS generation and NF‐κB activation in LPS‐stimulated BV2 microglial cells. This work was supported by grants from Korea Science and Engineering Foundation.