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Piceatannol attenuates lipopolysaccharide-induced NF-kappaB activation and NF-kappaB-related proinflammatory

Cheng-Yun Jin1, Dong-Oh Moon, Kyeong-Jun Lee

  • 1Department of Microbiology, College of Natural Sciences, Pusan National University, Busan 609-735, South Korea.

Pharmacological Research
|October 28, 2006
PubMed

Insights

Piceatannol (PIC) reduces key inflammatory molecules like nitric oxide (NO) and prostaglandin E(2) (PGE(2)) in brain cells. This natural compound shows potential for treating inflammatory brain conditions.

Area of Science:

  • Neuroscience
  • Immunology
  • Pharmacology

Background:

  • Proinflammatory mediators (PGE(2), NO, IL-1beta, IL-6, TNF-alpha) are crucial in brain injuries.
  • Anti-inflammatory responses involve downregulating these mediators post-injury.

Purpose of the Study:

  • To investigate the anti-inflammatory effects of piceatannol (PIC) on lipopolysaccharide (LPS)-stimulated BV2 microglia.
  • To determine PIC's impact on the production and expression of key inflammatory mediators and signaling pathways.

Main Methods:

  • BV2 microglia were stimulated with LPS.
  • The effects of varying concentrations of PIC on NO, PGE(2), and cytokine release were measured.
  • mRNA and protein levels of iNOS and COX-2 were assessed.
  • NF-kappaB p65 nuclear translocation was evaluated.

Main Results:

  • PIC significantly inhibited the release of NO, PGE(2), and proinflammatory cytokines in a dose-dependent manner.
  • PIC attenuated the expression of inducible NO synthase (iNOS) and cyclooxygenase (COX)-2 at mRNA and protein levels.
  • PIC prevented NF-kappaB p65 nuclear translocation, indicating suppression of this inflammatory pathway.

Conclusions:

  • Piceatannol exhibits significant anti-inflammatory properties in LPS-stimulated microglia.
  • PIC suppresses the transcription of proinflammatory cytokine genes via the NF-kappaB signaling pathway.
  • PIC's anti-inflammatory effects suggest potential therapeutic applications for inflammatory diseases and microglial activation.

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