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. 2016 May 9;7(23):33765–33782. doi: 10.18632/oncotarget.9260

Figure 3. Cisplatin-induced IL-10 production in LPS-activated DCs involved the activation of the p38 MAPK and NF-κB signaling pathways.

Figure 3

A. BMDCs were treated with LPS (100 ng/ml) in the absence or presence of cisplatin (5 μg/ml) for 0, 15, 30, 60, 120, and 240 min. Cell lysates were subjected to SDS-PAGE, and immunoblot analyses were performed using Abs specific to phospho-ERK1/2, phospho-JNK1/2 and phospho-p38. B., C. Cell lysates and nuclear lysates were subjected to SDS-PAGE, and immunoblot analyses were performed using Abs specific to phospho-IκB-α (p-IκB-α), non-phospho-IκB-α, and p65 NF-κB for 60 min. β-actin and lamin B were used as loading controls for the cytosolic and nuclear fractions, respectively. One representative plot out of three independent experiments is shown. D. BMDCs were treated with pharmacological inhibitors of p38 (SB203580), JNK (SP600125), or NF-κB (Bay11-7082) or DMSO (vehicle control) for 1 h prior to treatment with LPS in the absence or presence of cisplatin for 18 h. IL-10 levels in the culture medium were measured by ELISA. The values shown represent the mean ± SD from one representative plot out of three independent experiments; *p < 0.05, **p < 0.01, or ***p < 0.001 compared to DCs treated with LPS and cisplatin.