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. 2021 Sep 28;13(18):22588–22610. doi: 10.18632/aging.203572

Figure 5.

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.