Differential effects of triptolide and tetrandrine on activation of COX-2, NF-κB, and AP-1 and virus production in dengue virus-infected human lung cells

摘要: Most virus infections induce cycloxygenase-2 (COX-2) expression and subsequent prostaglandin E(2) (PGE(2)) production in cells, an inflammatory response that might be detrimental to replication pathogenesis. This dengue infection remains elucidated. Triptolide tetrandrine, compounds derived from two commonly used Chinese herbs, both demonstrate anti-inflammatory immunosuppressive effects partly through modulation of COX-2 and, hence, may have antiviral effects. In this study, we examined, firstly, the immune with respect PGE(2) human lung cells (A549), liver (HepG2) dendritic cells. Secondly, assessed potential triptolide tetrandrine on vis-a-vis COX-2, PGE(2), transcription factors, as well production. We found enhanced A549 similarly but not HepG2 virus-infected nuclear factor kappaB (NF-kappaB) activator protein 1 (AP-1) were also activated, dose-dependently inhibited by (0.5-4 ng/ml). Tetrandrine (1-10 microM) had no similar moreover, at higher concentrations, NF-kappaB AP-1 activity, However, unexpectedly, triptolide, suppressed independent level. Our findings imply attenuate distinct pathways.