Fig. 4From: NOD1/RIP2 signalling enhances the microglia-driven inflammatory response and undergoes crosstalk with inflammatory cytokines to exacerbate brain damage following intracerebral haemorrhage in miceNOD1 inhibition significantly reduced the inflammatory response in response to 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/ICH + DMSO group) and b, d in the 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 group); RIP2, total and phosphorylated JNK/P38 MAPK, and IκBα 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/ICH + DMSO) and f, h in the 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 group). All data are representative of three independent experimentsBack to article page