IL-8 and p53 are inversely regulated through JNK, p38 and NF-κB p65 in HepG2 cells during an inflammatory response

摘要

It is reported that Nuclear factor-κB (NF-κB) activation is dysregulated in chronic inflammatory diseases like psoriasis, rheumatoid arthritis and cancer, resulting in an over expression of pro-inflammatory cytokines and an inhibition of apoptosis. We studied NF-κB activation and the induction of interleukin 8 (IL-8) and p53 gene expression in an interleukin 1β (IL-1β) stimulated HepG2 cell line.