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. 2020 Dec 11;36(10):754–764. doi: 10.1089/jop.2020.0068

FIG. 6.

FIG. 6.

AMPK, but not PPARα, was implicated in the protective role of fenofibric acid on HOG-LDL-induced RPE barrier dysfunction. (A, B) Quiescent monolayer ARPE-19 cells were pretreated with vehicle control (DMSO), fenofibric acid (FA, 30 μM), FA (30 μM) + GW6471 (GW, 10 μM), or FA (30 μM) + Compound C (CompC, 10 μM) for 1 h, and then challenged with HOG-LDL (200 mg/L) for 6 h. TEER and FITC-dextran leakage were measured accordingly. Data are presented as percentage versus vehicle control (mean ± SD, n = 5). There was no significant difference between the HOG+FA+CompC treatment versus HOG-LDL treatment alone. (C) ARPE-19 cells were treated with FA (30 μM) for 0–12 h; p-AMPK and total AMPK were detected by Western blotting and densitometry. (D, E) ARPE-19 cells were pretreated with FA (30 μM), FA (30 μM) + GW6471 (10 μM), or FA (30 μM) + Compound C (10 μM) for 1 h, and then exposed to HOG-LDL (200 mg/L) for 6 h; N-LDL (200 mg/L) served as a control. Protein levels of LOX-1 and VEGF were detected by Western blotting and densitometry. Data are presented as percentages versus N-LDL (mean ± SD, n = 3 or 5). There was no significant difference between the HOG+FA+CompC treatment versus HOG-LDL treatment alone. VEGF, vascular endothelial growth factor; FA, fenofibric acid.