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

• Published in: The Korean journal of physiology & pharmacology 2012, Vol.16 (2), p.107-112
• Main Authors: Lee, Jae-Won, Bae, Chang-Jun, Choi, Yong-Jun, Kim, Song-In, Kim, Nam-Ho, Lee, Hee-Jae, Kim, Sung-Soo, Kwon, Yong-Soo, Chun, Wan-Joo
• Format: Article
• Language: Korean
• ISSN: 1226-4512; 2093-3827

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.