β-Carboline Alkaloid Suppresses NF-κB Transcriptional Activity Through Inhibition of IKK Signaling Pathway

Author： Woo Yoon Jong Ku Kang Jae Ro Lee Kang Woo Lee Hyang Whan Han Jeung Wan Seo Dong Kee Kim Yong

ISSN： 1087-2620

Source： Journal of Toxicology and Environmental Health, Vol.68, Iss.23-24, 2005-12, pp. : 2005-2017

Disclaimer: Any content in publications that violate the sovereignty, the constitution or regulations of the PRC is not accepted or approved by CNPIEC.

Previous Menu Next

Abstract

Nuclear factor (NF)-κB transcription factors play an evolutionarily conserved and critical role in the triggering and coordination of both innate and adaptive immune responses. Therefore, there is intense interest in understanding the regulation of this transcription factor in the context of various diseases. Studies investigated the suppression mechanism of NF-κB signaling pathways by a β-carboline alkaloid (C-1) in lipopolysaccharide (LPS)-stimulated RAW 264.7 cells. β-Carboline alkaloid decreased the level of inducible nitric oxide sythase (iNOS) protein and NOS promoter activities in a concentration-dependent manner. This effect was accompanied by the reduction of NF-κB DNA binding activity as well as NF-κB nuclear translocation. In addition, β-carboline alkaloid reduced the degradation and phosphorylation of IκB, and attenuated IKK activity in LPS-stimulated RAW 264.7 cells. Taken together, these results indicate that β-carboline alkaloid has the capability to suppress NF-κB signaling pathway through inhibition of IKK activity in LPS-stimulated RAW 264.7 cells.