Paeoniflorin reduced BLP-induced inflammatory response by inhibiting the NF-[kappa]B signal transduction in pathway THP-1 cells

Sepsis is a severe illness in which the bloodstream is overwhelmed by bacteria. Despite effective antibiotic treatment, the mortality of septic shock remains high. In this study, we examined a potential usage of paeoniflorin, anti-inflammatory component for the treatment of sepsis. We established an inflammatory cell line by stimulating human THP-1 cell line with bacterial lipoprotein (BLP), which resulted in an activation of nuclear factor κB (NF-κB) p65 dependent-signal pathway, and in consequence, an increase in tumor necrosis factor α (TNF-α) and interleukin (IL)-6 expression. With this model, we studied the effect of paeoniflorin on the expression of NF-κB and Toll-like receptor 2 (TLR2) mediated signal transduction. Our data indicated that paeoniflorin directly inhibited activation of NF-κB p65, thereby reduced the expression of TNF-α and IL-6 in the BLP stimulated THP-1 cells. Paeoniflorin was also found to inhibit IκB phosphorylation and degradation. However, no significant differences in TLR2 and myeloid differentiation factor 88 (MyD88) expression were observed; therefore, these signaling molecules may not have much anti-inflammatory effect in our cellular model. As such, our current study provided a molecular base for the potential use of paeoniflorin in therapeutic treatment of sepsis induced by bacterial lipoprotein.