Sauchinone suppresses lipopolysaccharide-induced inflammatory responses through Akt signaling in BV2 cells.

Abstract

Activated microglial cells play an important role in inflammatory responses in the central nervous system (CNS) that are involved in neurodegenerative diseases. Sauchinone has been shown to modulate the expression of inflammatory factors through nuclear factor-kappa B (NF-κB) signaling pathway. Here, we examined the effect of sauchinone on the inflammatory responses of microglia cells induced by lipopolysaccharide (LPS) and explored the mechanism underlying action of sauchinone. BV2 cells treated with LPS showed an up-regulation of nitric oxide (NO) and prostaglandin (PGE(2)) release, whereas sauchinone suppressed this up-regulation. Sauchinone inhibited both mRNA and protein expression of COX-2, iNOS, TNF-α and IL-1β. In addition, sauchinone blocked the activation of NF-κB through its inhibition of I-κB phosphorylation. Interestingly, sauchinone had no effect on the LPS-induced phosphorylation of mitogen activated protein kinases (MAP kinases; ERK1/2, p38, JNK), but it did inhibit Akt phosphorylation. These results suggest that the inhibitory effect of sauchinone on the LPS-induced production of inflammatory mediator in BV2 cells is associated with the suppression of the NF-κB and Akt signaling pathways. Therefore, sauchinone may be a useful treatment for neurodegenerative disease by inhibiting inflammatory responses in activated microglia.

• Authors: Eun Young Jang, Chae Ha Yang, Min Ho Han, Yung Hyun Choi, Meeyul Hwang
• Journal: International immunopharmacology (Int Immunopharmacol) Vol. 14 Issue 2 Pg. 188-94 (Oct 2012) ISSN: 1878-1705 [Electronic] Netherlands
• PMID: 22824073 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
• Copyright: Copyright © 2012 Elsevier B.V. All rights reserved.

Chemical References

• Benzopyrans
• Dioxoles
• Inflammation Mediators
• Lipopolysaccharides
• NF-kappa B
• sauchinone
• Nitric Oxide
• Oncogene Protein v-akt
• Dinoprostone

Topics

• Animals
• Benzopyrans (pharmacology)
• Cell Line
• Dinoprostone (metabolism)
• Dioxoles (pharmacology)
• Humans
• Immunosuppression Therapy
• Inflammation (immunology)
• Inflammation Mediators (metabolism)
• Lipopolysaccharides (immunology)
• Mice
• Microglia (drug effects, immunology)
• NF-kappa B (metabolism)
• Neurodegenerative Diseases (immunology)
• Nitric Oxide (metabolism)
• Oncogene Protein v-akt (metabolism)
• Signal Transduction (drug effects)