Skip to main content
. Author manuscript; available in PMC: 2013 Mar 1.
Published in final edited form as: J Neurochem. 2012 Feb 6;120(6):1060–1071. doi: 10.1111/j.1471-4159.2012.07660.x

Figure 2. Effects of inhibitors of TLR4, CD36, and acyl-CoA synthetase on palmitic acid-induced TNFα and IL-6 release.

Figure 2

Primary astrocytes were with vehicle (BSA) or 200 μM palmitic acid (PA) in the presence or absence of a pharmacologic inhibitor of TLR4 (TAK-242, 5 μM), neutralizing antibodies to CD36 (FA6.152, 20 μg/ml), or a pharmacologic inhibitor of acyl-CoA synthetase (Triacsin C, 10 μM). All inhibitors were applied to cells 45 min before administration of BSA or palmitic acid. Release of (A) TNFα, (B) IL-6, and (C) MTT conversion to formazan was measured after 24 h. Data were compiled from 2–4 separate experiments, and are means and SEM of 10–20 dishes per group. *** indicates significant (p<0.001) increases in cytokine release from astrocytes treated with palmitic acid as compared to control cells treated with just BSA, and ### indicates significant (p<0.001) decreases in cytokine release from astrocytes treated with palmitic acid in the presence of TAK-242 as compared to cells treated with palmitic acid alone.