Methylalpinumisoflavone Inhibits Lipopolysaccharide-Induced Inflammation in Microglial Cells by the NF-kappaB and MAPK Signaling Pathway
Article first published online: 16 AUG 2012
Copyright © 2012 John Wiley & Sons, Ltd.
Volume 26, Issue 12, pages 1948–1956, December 2012
How to Cite
Lim, J.-Y., Hwang, B. Y., Hwang, K.-W. and Park, S.-Y. (2012), Methylalpinumisoflavone Inhibits Lipopolysaccharide-Induced Inflammation in Microglial Cells by the NF-kappaB and MAPK Signaling Pathway. Phytother. Res., 26: 1948–1956. doi: 10.1002/ptr.4810
- Issue published online: 11 DEC 2012
- Article first published online: 16 AUG 2012
- Manuscript Accepted: 23 JUL 2012
- Manuscript Revised: 8 JUL 2012
- Manuscript Received: 9 AUG 2011
- anti-inflammatory effect;
- BV2 cells
Neuroinflammation is chronic inflammation within the brain that is attributed to prolonged activation of microglial cells and results in neurodegenerative events, such as neuronal dysfunction and neuronal loss. Therefore, suppression of neuroinflammation would theoretically slow progression of neurodegenerative disease. In this study, we investigated the anti-inflammatory effects of 4′-O-methylalpinumisoflavone (methylalpinumisoflavone), isolated from Cudrania tricuspidata, against LPS-induced microglial activation in BV2 cells. Exposure of BV2 cells to LPS (0.5 µg/mL) significantly increased production of pro-inflammatory mediators, including NO, PGE2, and pro-inflammatory cytokines. Conversely, pre-treatment with methylalpinumisoflavone (10 and 20 µg/mL) prior to treatment with LPS resulted in a significant decrease of LPS-induced production of pro-inflammatory mediators in a dose-dependent manner. In addition, reduction of pro-inflammatory mediators by treatment with methylalpinumisoflavone prior to treatment with LPS was accompanied by a decrease in translocation of NF-κB p50 and p65 from the cytoplasm to the nucleus and by a decrease in activation of mitogen-activated protein kinases (MAPKs), such as ERK1/2 and JNK. Taken together, these results suggest that methylalpinumisoflavone suppressed LPS-induced microglial activation and production of pro-inflammatory mediators by decreasing NF-κB signaling and by phosphorylation of MAPKs. These results suggest the potential of methylalpinumisoflavone as an anti-inflammatory drug candidate. Copyright © 2012 John Wiley & Sons, Ltd.