Fig. 9

Effect of MAPK inhibitors on HSP60-induced inflammation in N9 microglial cells. N9 cells were cultured in the presence or absence of MAPK inhibitors; U0126 (10 μM), SP600125 (10 μM), and SB203580 (10 μM) 60 min prior to transfection of 4 μg of HSP60 cDNA clone and then incubated for 24 h. a–c The effect of ERK inhibitor U0126, JNK inhibitor SP600125 (SP), and p38 inhibitor SB0193 (SB) on phospho- and total ERK1/2 (a), on phospho- and total JNK (b), on phospho- and total p38 (c), respectively, and on pro-inflammatory molecules iNOS and COX2 (a–c). Right panel (a–c) shows bar graphs which represent mean fold change in iNOS and COX2 with respect to control, in different treatment conditions. The blots are representative of three independent experiments. One hundred microgram protein was loaded for western blots, and β-actin was used as a loading control. d Effect of specific inhibition of MAPKs on pro-inflammatory cytokines. CBA analysis of TNF-α, MCP-1, and IL-6 after treatment of N9 microglial cells with U0126, SP600125, and SB203580 inhibitors (i–iii). Data represented are mean ± SD of three independent experiments. *p < 0.05, **p < 0.01 in comparison to control values