GPR40 activation by CNX-011-67 reduces cellular inflammation. Western blot of NIT1 cells treated with inflammatory cytokines in presence or absence of GPR40 agonist (A, B). Inflammatory cytokines (TNFα + IL1β) increased JNK phosphorylation (A) and reduced IκB level (B) in NIT1 cells which were reversed by GPR40 activation. Total JNK and β-actin were used as loading control for normalization. Expression of NF-κB (C), IL1β (D), TNFα (E) and NOS2a (F) genes were up-regulated under inflammatory conditions and were down-regulated by GPR40 activation in rat islets. Gene expression was measured by qRT-PCR. (n = 4, **P < 0.01, ***P < 0.001).