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. 2017 Dec 18;9(12):1370. doi: 10.3390/nu9121370

Figure 1.

Figure 1

Palmitate (PA) induces NLRP3 inflammasome activation. (A) THP-1 cells were treated with 200 μM PA for 2, 4, 8, 12, and 24 h. The mRNA levels of NLRP3, caspase-1, interleukin (IL)-18, and IL-1β were examined by quantitative RT-PCR; (B) THP-1 cells were treated with 200 μM PA for 4, 8, 12, and 24 h. Cell lysates and supernatants were subjected to immunoblotting using antibodies specific for NLRP3, caspase-1, IL-18, IL-1β, and β-actin. Relative protein levels were analyzed with ImageJ; (C,D) The levels of caspase-1 and IL-1β in the culture supernatants were determined by ELISA; (E–H) Primary murine macrophages were treated with 200 μM PA for 12 h; (E) The mRNA levels of NLRP3, caspase-1, IL-18, and IL-1β were measured by quantitative RT-PCR; (F) Cell lysates and supernatants were subjected to immunoblotting using antibodies specific for NLRP3, caspase-1, IL-18, IL-1β, and β-actin. Relative protein levels were analyzed with ImageJ; (G, H) The levels of caspase-1 and IL-1β in the culture supernatants were determined by ELISA. * p < 0.05 compared with PA-untreated cells.