Figure 8.

NF-κB, JAK-STAT and JNK kinase inhibition prevent LPS- induced iNOS and protect from LPS -induced injury in BV2 and bEND.3 coculture model. Panel A: LPS treatment of bEND.3/BV2 cocultures (LPS) increased cell death and disruption of bEND.3 monolayers compared to control cocultures (Control). Treatment with inhibitors to block JNK (SP600125), JAK-STAT (AG490) or NF-κB (PDTC) reduced this disruption, whereas treatment with a MEK1 inhibitor (PD98059) did not. Panels B & C summarize the effect of these various inhibitors on LPS-induced cell viability (B) and NO accumulation (C). These data show that inhibition of JNK, JAK-STAT and NF-κB improve cell viability while decreasing NO accumulation, whereas inhibition of MEK1, p38 MAPK (SB 203580) and PI3K (wortmannin) do not. CTL: control cultures treated with vehicle. (n = 12 independent observations), *P < 0.05vs. control, # P < 0.05 versus LPS).

Kacimi et al. Journal of Inflammation 2011 8:7   doi:10.1186/1476-9255-8-7
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