Anti-inflammatory effects of Polygala tenuifolia root through inhibition of NF-kappa B activation in lipopolysaccharide-induced BV2 microglial cells

作者:Cheong Myung Hee; Lee Sang Ryong; Yoo Hwa Seung; Jeong Jin Woo; Kim Gi Young; Kim Wun Jae; Jung In Chul*; Choi Yung Hyun
来源:Journal of Ethnopharmacology, 2011, 137(3): 1402-1408.
DOI:10.1016/j.jep.2011.08.008

摘要

Ethnopharmacological relevance: The root of Polygala tenuifolia Willd is a well-known traditional Oriental medicine and has been prescribed for treatment of dysfunction in memorial systems and various brain inflammatory diseases. The present study was designed to validate the anti-inflammatory effects of the water extract of Polygala tenuifolia root (WEPT). Materials and methods: The anti-inflammatory properties of WEPT were studied using lipopolysaccharide (LPS)-stimulated murine BV2 microglia model. As inflammatory parameters, the production of nitric oxide (NO), inducible NO synthase (iNOS), cyclooxygenase (COX)-2, prostaglandin E(2) (PGE(2)), tumor necrosis factor (TNF)-alpha, and interleukin (IL)-1 beta were evaluated. We also examined the extract's effect on the activity of nuclear factor-kappaB (NF-kappa B), and toll-like receptor 4 (TLR4) and myeloid differentiation factor 88 (Myd-88) expression. Results: WEPT suppressed LPS-induced production of NO, PGE(2), and expression of iNOS and COX-2 in a dose-dependent manner, without causing cytotoxicity. It also significantly reduced generation of proinflammatory cytokines, including IL-1 beta and TNF-alpha. In addition, WEPT suppressed NF-kappa B translocation by blockade of IkappaB-alpha (I kappa B-alpha) degradation and inhibited TLR4 and Myd-88 expression in LPS-stimulated BV2 cells. Conclusions: These results indicate that the inhibitory effects of WEPT on LPS-stimulated inflammatory mediator production in BV2 microglia are associated with suppression of the NF-kappa B and toll-like receptor signaling pathways. Therefore, Polygala tenuifolia extracts may be useful in treatment of neurodegenerative diseases by inhibition of inflammatory mediator production in activated microglia.

  • 出版日期2011-10-11