Research Paper Volume 13, Issue 18 pp 22588—22610

GPR43 regulation of mitochondrial damage to alleviate inflammatory reaction in sepsis


Figure 5. P47phox caused ROS production in the function of GPR43 in sepsis-induced inflammatory reactions model. Survival rate (A) in GRP43-/- mice with CLP and anti-p47phox for 72 h; W/D rate (B), lung injury score (C), lung tissue using HE staining (D), SOD activity level (E), serum IL-1β levels (F), NLRP3/caspase-1/ IL-1β protein expressions (G) in GRP43-/- mice with CLP and anti-p47phox for 24 h; NLRP3, Caspase-1 and IL-1β protein expressions in cells and IL-1β protein expression in supernatant (H), IL-1β levels (I), 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-/-+ROS i, GPR43-/- mice of CLP with ROS inhibitor; Negative, negative control; Si-GPR43, down-regulation of GPR43; si-p47phox, down-regulation of p47phox; 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.