Suppression of LPS-induced inflammatory responses by inflexanin B in BV2 microglial cells

Ji Youn Lim, Donggeun Sul, Bang Yeon Hwang, Kwang Woo Hwang, Ki Yeol Yoo, So Young Park

Research output: Contribution to journalArticlepeer-review

7 Citations (Scopus)

Abstract

Microglia are a type of resident macrophage that functions as an inflammation modulator in the central nervous system. Over-activation of microglia by a range of stimuli disrupts the physiological homeostasis of the brain, and induces inflammatory response and degenerative processes, such as those implicated in neurodegenerative diseases, including Alzheimer's disease and Parkinson's disease. Therefore, we investigated the possible anti-inflammatory mechanisms of inflexanin B in murine microglial BV2 cells. Lipopolysaccharide (LPS) activated BV2 cells and induced the production of pro-inflammatory mediators such as nitric oxide (NO), prostaglandin E2 (PGE2), and cytokines (interleukins-1β and -6, and tumour necrosis factor α). The LPS-induced production of pro-inflammatory mediators was associated with the enhancement of nuclear factor-kappaB (NF-κB) nuclear translocation and the activation of mitogen-activated protein kinase (MAPK) including ERK1/2 and JNK. Conversely, pretreatment of cells with inflexanin B (10 and 20 μg/mL) significantly reduced the production of pro-inflammatory mediators. This was accompanied with the reduced nuclear translocation of NF-κB and reduced activation of MAPKs. These results suggest that inflexanin B attenuated the LPS-induced inflammatory process by inhibiting the activation of NF-κB and MAPKs.

Original languageEnglish
Pages (from-to)141-148
Number of pages8
JournalCanadian Journal of Physiology and Pharmacology
Volume91
Issue number2
DOIs
Publication statusPublished - 2013 Feb

Keywords

  • Anti-inflammatory effect
  • Inflexanin B
  • Microglial cells
  • NF- and κB

ASJC Scopus subject areas

  • Physiology
  • Pharmacology
  • Physiology (medical)

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