Research Paper Volume 13, Issue 18 pp 22588—22610

Figure 8. GPR43 is involved in the activation of NLRP3 inflammasome in sepsis model by PPARγ. Survival rate (A) in GRP43^-/- mice with CLP and PPARγ a for 72 h; W/D rate (B), lung injury score (C), lung tissue using HE staining (D), serum IL-1β levels (E), PPARγ/NOX-1/EBP50/ p47phox/NLRP3/caspase-1/ IL-1β protein expressions (F) in GRP43^-/- mice with CLP and PPARγ a for 24 h; PPARγ, NOX-1, EBP50, p47phox, NLRP3, Caspase-1 and IL-1β protein expressions in cells and IL-1β protein expression in supernatant (G, I), IL-1β levels (H), ROS production level (J), and SOD activity levels (K) in macrophage by down-regulation of GPR43 and LPS+ATP+GPR43 agonist for 24 h. GPR43^-/-, GPR43^-/- mice with CLP; GPR43^-/-+ PPARγ a, GPR43^-/- mice of CLP with PPARγ a; Negative, negative control; Si-GPR43, down-regulation of GPR43; PPARγ a, Pioglitazone; LPS+ATP+4-CMTB, macrophage by treated with LPS+ATP+4-CMTB. ##p<0.01 compared with GPR43^-/- mice with CLP or GPR43^-/- mice with CLP; **p<0.01 compared with down-regulation of GPR43.