Fig. 5

RIP2 inhibition alleviated the inflammatory response induced by NOD1 activation post ICH. Levels of iNOS, TNF-α, and IL-1β protein a, c in the brain in the indicated groups (n = 3 mice for each group; *P < 0.01 vs. the sham group, **P < 0.01 vs. the ICH + iE group, #P < 0.01 vs. the ICH + DMSO, ##P < 0.01 vs. the Hemin + iE group) and b, d in cultured primary microglia from the indicated groups (n = 3 experiments for each group; *P < 0.01 vs. the ctrl group, **P < 0.01 vs. the Hemin + iE group, #P < 0.01 vs. the Hemin + DMSO, ##P < 0.01 vs. the Hemin + iE group). Total and phosphorylated JNK/P38 MAPK, IκBα, and NOD1 protein levels e, g in the brain in the indicated groups (n = 3 mice for each group; *P < 0.01 vs. the sham group, **P < 0.01 vs. the ICH + iE group, #P < 0.01 vs. the ICH + DMSO, ##P < 0.01 vs. the Hemin + iE group) and f, h in cultured primary microglia from the indicated groups (n = 3 experiments for each group; *P < 0.01 vs. the ctrl group, **P < 0.01 vs. the Hemin + iE group, #P < 0.01 vs. the Hemin + DMSO, ##P < 0.01 vs. the Hemin + iE group). All data are representative of three independent experiments