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3,4,5-Trihydroxycinnamic Acid Inhibits LPS-Induced iNOS Expression by Suppressing NF-${\kappa}B$ Activation in BV2 Microglial Cells

  • Lee, Jae-Won (Department of Pharmacology, College of Medicine, Kangwon National University) ;
  • Bae, Chang-Jun (Department of Laboratory Animal Resources, National Institute of Food and Drug Evaluation, Korea FDA) ;
  • Choi, Yong-Jun (Department of Pharmacology, College of Medicine, Kangwon National University) ;
  • Kim, Song-In (Department of Pharmacology, College of Medicine, Kangwon National University) ;
  • Kim, Nam-Ho (Department of Pharmacology, College of Medicine, Kangwon National University) ;
  • Lee, Hee-Jae (Department of Pharmacology, College of Medicine, Kangwon National University) ;
  • Kim, Sung-Soo (Department of Pharmacology, College of Medicine, Kangwon National University) ;
  • Kwon, Yong-Soo (College of Pharmacy, Kangwon National University) ;
  • Chun, Wan-Joo (Department of Pharmacology, College of Medicine, Kangwon National University)
  • Received : 2011.12.29
  • Accepted : 2012.04.03
  • Published : 2012.04.30

Abstract

Although various derivatives of caffeic acid have been reported to possess a wide variety of biological activities such as neuronal protection against excitotoxicity and anti-inflammatory property, the biological activity of 3,4,5-trihydroxycinnamic acid (THC), a derivative of hydroxycinnamic acids, has not been clearly examined. The objective of the present study is to evaluate the anti-inflammatory effects of THC on lipopolysaccharide (LPS)-stimulated BV2 microglial cells. THC significantly suppressed LPS-induced excessive production of nitric oxide (NO) and expression of iNOS, which is responsible for the production of iNOS. THC also suppressed LPS-induced overproduction of pro-inflammatory cytokines such as IL-$1{\beta}$and TNF-${\alpha}$ in BV2 microgilal cells. Furthermore, THC significantly suppressed LPS-induced degradation of $I{\kappa}B$, which retains NF-${\kappa}B$ in the cytoplasm. Therefore, THC attenuated nuclear translocation of NF-${\kappa}B$, a major pro-inflammatory transcription factor. Taken together, the present study for the first time demonstrates that THC exhibits antiinflammatory activity through the suppression of NF-${\kappa}B$ transcriptional activation in LPS-stimulated BV2 microglial cells.

Keywords

References

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