Myricitrin Modulates NADPH Oxidase-Dependent ROS Production to Inhibit Endotoxin-Mediated Inflammation by Blocking the JAK/STAT1 and NOX2/p47^phox Pathways

Figure 3

Noncytotoxic level of myricitrin inhibited LPS-induced JAK and STAT activation but had no impact on MAPKs phosphorylation. RAW264.7 cells were stimulated with LPS for (a) 0, 5, 10, 15, 20, 25, 30, 35, 40, 45, 50, and 60 min; (c) 0, 2, 5, 10, 15, and 30 min; and (d) 0, 0.5, 1, 2, 4, and 6 h. In addition, RAW264.7 cells were pretreated with myricitrin at 100, 200, and 400 μg/ml for 2 h and then stimulated with LPS for 30 min (b), 15 min (e), and 4 h (f). Total protein was subjected to 10% SDS-PAGE followed by western blotting using specific antibodies against phospho-ERK, phospho-JNK, and phospho-P38 (a, b); phospho-JAK1 and phospho-JAK2 (c, e); and phospho-STAT1 and phospho-STAT3 (d, f). Nonphosphorylated antibodies were the internal control. Each value indicated the mean ± SD and was a representative of the results obtained from three individual experiments. versus LPS-stimulated groups.

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