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.
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