Fig. 6

Genetic deletion or pharmacological inhibition of sEH attenuated thrombin- and hemin-induced microglial activation and proinflammatory responses in cultured microglia. a Effects of sEH deletion on thrombin- or hemin-induced release of NO at 24 h from the supernatant of primary microglial cultures and b BV2 microglial cultures. c Effects of AUDA and pan-EET receptor antagonist 14,15-EEZE (1 μM) on thrombin- or hemin-induced release of NO at 24 h from the supernatants of primary microglial cultures. Effects of AUDA on d thrombin- or e hemin-induced release of IL-1β, IL-6, and MIP-2 at 24 h from the supernatant of primary mouse microglial cultures. Representative immunoblots and quantitative data of f iNOS and g COX-2 protein levels following co-treatment of 10 μM AUDA with thrombin or hemin at 6 and 24 h in BV2 microglia. Values are mean ± S.E.M.; ^# P < 0.05, ^## P < 0.01, and ^{###, †††} P < 0.001 vs. control group; *P < 0.05, **P < 0.01, and ***P < 0.001 vs. thrombin- or hemin-stimulation group; ^††† P < 0.001 vs. thrombin- or hemin-stimulation + AUDA group (n = 4 experiments/group for NO levels, n = 3 experiments/group for ELISA, and n = 4–5 mice/group for Western blot, one-way ANOVA, or repeated measures two-way ANOVA)