Fig. 6

NOD1 and RIP2 expression can be upregulated by IL-1β and TNF-α. Total and phosphorylated JNK/P38 MAPK, IκBα, NOD1, and RIP2 protein levels a, c in the brain in ICH-induced mice treated with the indicated inhibitors (n = 3 mice for each group; *P < 0.01 vs. the sham group, #P < 0.01 vs. the ICH + DMSO group) and b, d in hemin-challenged BV2 cells pretreated with the indicated inhibitors (n = 3 experiments for each group; *P < 0.01 vs. the ctrl group, #P < 0.01 vs. the Hemin + DMSO group). NOD1 and RIP2 expression e, g in primary microglia challenged with either TNF-α or IL-1β alone or in combination for 24 h (n = 3 experiments for each group; *P < 0.01 vs. the ctrl group, #P < 0.01 vs. the IL-1β + TNF-α-challenged group) and f, h in mice challenged with either TNF-α or IL-1β alone or in combination for 24 h (n = 3 mice for each group; *P < 0.01 vs. the sham group, #P < 0.01 vs. the IL-1β + TNF-α-challenged group). All data are representative of three independent experiments