Research Paper Volume 13, Issue 18 pp 22588—22610

GPR43 regulation of mitochondrial damage to alleviate inflammatory reaction in sepsis


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.