and Their NF-κB Inhibitory Activity in HepG2 Cells

Nuclear transcription factor-κB (NF-κB) represents a family of Rel domain-containing proteins including RelA, RelB, c-Rel, NF-κB1, and NF-κB2. The activation of NF-κB has been linked to multiple pathophysiological conditions such as cancer, arthritis, asthma, inflammatory bowel di-sease, and other inflammatory conditions.1 NF-κB can be activated by various stimuli, such as microbial and viral products, cytokines, DNA damage and noxious chemicals. The induction of a number of pro-inflammatory mediators occurs as the results of increased inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) activities.2 Therefore, suppression of iNOS and COX-2 activities can be an important approach to preventing inflammation in organs. NF-κB and the signaling pathways that regulate many physiological processes, including the innate- and adaptive