Fig. 7

TLR4 plays a pivotal role in HSP60-induced inflammation in microglia. N9 cells were cultured in the presence or absence of 10 μM TLR4 inhibitor (CLI-095) 2 h prior to transfection of mouse HSP60 plasmid clone. a Left panel shows western blots illustrating effect of TLR4 inhibitor on iNOS and COX2 in the cells transfected with 4 μg mouse HSP60 plasmid clone or control pCMV6 plasmid, right panel represents the bar diagrams which reflect mean fold change in expression as compared to control. One hundred microgram protein was loaded for western blots of iNOS and COX2, and β-actin was used as a loading control. The blots are representative of three independent experiments. b CBA analysis of pro-inflammatory cytokines (TNF-α, MCP-1, and IL-6) also suggests a major involvement of TLR4 in HSP60-induced inflammation in microglia. Bar diagrams are mean fold change of three independent experiments with similar results. Data represented are mean ± SD of three independent experiments. *p < 0.05, **p < 0.01 in comparison to control values and ^# p < 0.01 in comparison to IL-1β treatment