Fig. 5From: NOD1/RIP2 signalling enhances the microglia-driven inflammatory response and undergoes crosstalk with inflammatory cytokines to exacerbate brain damage following intracerebral haemorrhage in miceRIP2 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 experimentsBack to article page