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. 2020 Jun 2;36:101591. doi: 10.1016/j.redox.2020.101591

Fig. 1.

Fig. 1

NO2-OA regulates CD36 expression in RAW 264.7 macrophages and BMDM. A. Density plots of CD36 in RAW264.7 macrophages stimulated with increasing concentrations of NO2-OA (0–5.0 μM) for 8 h (Side Scatter-A vs CD36-APC fluorescence). B. Time course effect of NO2-OA or OA (5 μM) on CD36 mRNA expression in RAW264.7 macrophages. C. CD36 and HO-1 expression in macrophages incubated with NO2-OA (0–5 μM) or CDDO-Me (300 nM) for 8 h. GAPDH was used as a loading control. D. NO2-OA induction of CD36 expression. Macrophages were pre-incubated with 10 μM of the PPARγ antagonist GW9662 or 10 μM of the agonist rosiglitazone during 10 min or 20 min with the Nrf2 activator CDDO-Me (300 nM) before NO2-OA addition. E and F. CD36 expression in BMDM from Nrf2-KO mice. Protein (HO-1, NQO1 and CD36) and mRNA levels (CD36) of BMDM obtained from WT and Nrf2-KO mice were treated with 5 μM of NO2-OA, 5 μM OA or 300 nM of CDDO-Me (8 h for Western blot analysis and 4 h for RT-qPCR analysis). The data is a representative experiment selected from at least 3 independent experiments, n = 3- for each determination showing mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001.