14:T4b5,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.
15:T4f4,Nox1/EBP50/p47phox is involved in the activation of NLRP3 inflammasome by GRP43 gene in sepsis model. EBP50 and p47phox sequence structures highlighting the PDZ domains of EBP50 and the potential PDZ-binding motif on p47phox, streptavidin regulated anti-p47phox or anti-EBP50 antibodies on RAW264.7 cell (A); Anti-FLAG antibody with anti-p47phox or anti-FLAG antibodies on lysates (B); P47phox and EBP50 expression in vitro model using confocal (C); Outline of p47phox sequence structures highlighting the mutation (in red) of C-terminal PDZ binding motif on p47phox (D); NOX-1 and p47phox sequence structures highlighting the PDZ domains of NOX-1 and the potential PDZ-binding motif on p47phox (E); Anti-FLAG antibody with anti- NOX-1 or anti-FLAG antibodies on lysates (F); NOX-1 and EBP50 expression in vitro model using confocal (G); Nox1, EBP50 and p47phox protein expressions in macrophage by down-regulation of GPR43 and LPS+ATP+GPR43 agonist (H, I). Control, control group; LPS+ATP, macrophage by treated with LPS+ATP; L-4-CMTB, 10 μM of 4-CMTB; M-4-CMTB, 20 μM of 4-CMTB; H-4-CMTB, 40 μM of 4-CMTB. ##p<0.01 compared with control group; **p<0.01 compared with LPS+ATP.
16:T4b0,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.