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. Author manuscript; available in PMC: 2015 Apr 1.
Published in final edited form as: Hepatology. 2014 Mar 3;59(4):1543–1554. doi: 10.1002/hep.26625

Figure 2. Different effects of broad-spectrum versus classical PKC inhibitors on p-JNK levels and p-AMPK levels following APAP treatment in primary cultured hepatocytes.

Figure 2

Figure 2

A) Time course of JNK phosphorylation following APAP treatment (2 h) in hepatocytes. Hepatocytes were treated with APAP for 2 hours, then APAP was removed and hepatocytes incubated in fresh media without APAP for another 2-6 hours (post-APAP). B) Effect of broad-spectrum PKC inhibitors - Ro-31-8425 (5 μM), Go6983 (10 μM) or classical PKC inhibitor - Go6976 (10 μM) on JNK phosphorylation in hepatocytes following APAP treatment. C) Time course of p-AMPK following APAP treatment in hepatocytes. Hepatocytes were treated with APAP for 2 hours, then APAP was removed and hepatocytes incubated in fresh media without APAP for another 2-4 hours (post-APAP). D) Effect of broad-spectrum PKC inhibitors - Ro-31-8425 (5 μM), Go6983 (10 μM) or classical PKC inhibitor - Go6976 (10 μM) on p-AMPK levels in hepatocytes following APAP treatment. In the time course experiments, hepatocytes were treated with APAP (25 mM) for two hours, APAP was removed, and hepatocytes were incubated in fresh media without APAP for the times indicated (post-APAP). In experiments involving PKC inhibitors, hepatocytes were treated with APAP (25 mM) for 2 h, then APAP was removed, and the cells were treated with different PKC inhibitors or DMSO for control for another 2 h. Western blot analyses were performed using antisera against p-JNK, JNK, p-AMPK (Thr 172), AMPK and β-Actin. Densitometry was determined using Image J. Results are mean ± S.D. * p value ≤ 0.05 versus control; # p value ≤ 0.05 versus APAP treatment alone.