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. 2015 May 7;146(2):265–280. doi: 10.1093/toxsci/kfv091

FIG. 7.

FIG. 7.

ERK is involved in the NSAID/cytokine-induced cytotoxic interaction. HepG2 cells were treated with (A) AA derivatives (DCLF: 250 µM, BRM: 750 µM or SLD sulfide: 200 μM), or (B) PA derivatives (IBU: 6 mM or NAP: 10 mM) alone or in combination with TNFα and/or IFNγ. NSAID/cytokine combinations were also incubated in the presence and absence of the ERK inhibitor U0126 (20 μM). Cytotoxicity was measured 24 h later. (C) Cells were treated with a representative AA derivative (DCLF: 250 µM) or a representative PA derivative (IBU: 6 mM) in the presence or absence of U0126 for 12 h and p-ERK and total ERK protein was detected via western analysis. a, significantly different from VEH within NSAID/inhibitor treatment; b, significantly different from TNFα within NSAID/inhibitor treatment; c, significantly different from Control within a cytokine group; d, significantly different from NSAID without inhibitor within a cytokine group. Data are represented as mean ± S.E.M of at least 5 separate experiments. VEH, vehicle; TNF, tumor necrosis factor-alpha; IFN, interferon-gamma; LDH, lactate dehydrogenase; DCLF, diclofenac; BRM, bromfenac; SLD, sulindac; IBU, ibuprofen; NAP, naproxen; U0, U0126.