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. Author manuscript; available in PMC: 2020 Dec 15.
Published in final edited form as: Cancer Res. 2020 Mar 25;80(12):2564–2574. doi: 10.1158/0008-5472.CAN-19-3184

Figure 5.

Figure 5.

A-FABP is critical in n-3 FA-mediated ROS production and macrophage cell death. A, B, BMMs from WT and A-FABP−/− mice were treated with DPA for 30mins. Mitochondrial potential was measured by flow cytometry with MitoSpy staining (A). Relative MFI of MitoSpy is shown in panel B. C, extracellular flux analysis of OCR in DPA-treated BMMs from WT and A-FABP−/− mice in the presence of injected drugs at the indicated time points. D, measurement of fluorescent intensity of DCFDA in WT or A-FABP−/− BMMs treated with DPA (200μM) for 30 mins by flow cytometry. E, confocal microscopy analysis of ROS production (green) in WT and A-FABP−/− BMMs treated with DPA for 30 mins. F-G, WT and A-FABP−/− BMMs were treated with DPA 12h, respectively. Real-time PCR analysis of expression of Cpt1b (F), iNOS (G), Caspase 8 (H) and Caspase 11 (I) in these cells. J, flow analysis of ROS levels in A-FABP−/− BMMs treated with 200 μM DPA in the presence or absence of 1mM NAC for 30 mins. K, flow cytometric analysis of DPA-induced A-FABP−/− BMM cell death with or without NAC treatment. Experiments were repeated three times. Data are shown as mean ± SD (*p<0.05; **p<0.01 as compared to BSA group).