Figure 7
Proposed model for CBX-mediated inhibition of HMGB1 release. Prolonged stimulation with crude LPS may lead to panx-1 hemichannel-mediated ATP efflux, and upregulation of PKR expression. Extracellular ATP then binds to P2X7R and activates the ATP-gated P2X7R and panx-1 channels, leading to PKR phosphorylation and subsequent inflammasome-dependent HMGB1 release. As a panx-1 inhibitor, CBX may block LPS-induced ATP efflux, thereby impairing ATP/P2X7R-mediated PKR activation, and subsequent inflammasome-dependent HMGB1 release.