3,4,5-Trihydroxycinnamic Acid Inhibits LPS-Induced iNOS Expression by Suppressing NF-kappaB Activation in BV2 Microglial Cells.
10.4196/kjpp.2012.16.2.107
- Author:
Jae Won LEE
1
;
Chang Jun BAE
;
Yong Jun CHOI
;
Song In KIM
;
Nam Ho KIM
;
Hee Jae LEE
;
Sung Soo KIM
;
Yong Soo KWON
;
Wanjoo CHUN
Author Information
1. Department of Pharmacology, College of Medicine, Kangwon National University, Chuncheon 200-701, Korea. wchun@kangwon.ac.kr
- Publication Type:Original Article
- Keywords:
3,4,5-Trihydroxycinnamic acid (THC);
BV2 microglial cells;
Lipopolysaccharide;
iNOS;
NF-kappaB
- MeSH:
Caffeic Acids;
Coumaric Acids;
Cytokines;
Cytoplasm;
Neurons;
NF-kappa B;
Nitric Oxide;
Tetrahydrocannabinol;
Transcription Factors;
Transcriptional Activation;
Tumor Necrosis Factor-alpha
- From:The Korean Journal of Physiology and Pharmacology
2012;16(2):107-112
- CountryRepublic of Korea
- Language:English
-
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-1beta and TNF-alpha in BV2 microgilal cells. Furthermore, THC significantly suppressed LPS-induced degradation of IkappaB, which retains NF-kappaB in the cytoplasm. Therefore, THC attenuated nuclear translocation of NF-kappaB, a major pro-inflammatory transcription factor. Taken together, the present study for the first time demonstrates that THC exhibits anti-inflammatory activity through the suppression of NF-kappaB transcriptional activation in LPS-stimulated BV2 microglial cells.
