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. 2009 Aug 19;297(5):F1399–F1410. doi: 10.1152/ajprenal.00051.2009

Fig. 10.

Fig. 10.

Effect of the NADPH oxidase inhibitor DPI on oxalate- or PMA-induced H2O2 production, LDH release, and PKC activity. A and B: LLC-PK1 cells were pretreated with 0.5 μM DPI for 30 min and then exposed to 0.75 mM oxalate or 1 μM PMA along with DPI for 3 h, after which H2O2 production (A) and LDH release (B) were determined. DMSO was used as a vehicle. Data are normalized to control, and values are expressed as means ± SE. Comparisons shown: a, significant compared with control; b, significant compared with oxalate-treated; c, significant compared with PMA-treated; d, significant compared with DPI-treated control.*P < 0.05; n = 6. C: effect of DPI on oxalate-induced PKC activity in the membrane fraction. LLC-PK1 cells were pretreated with 0.5 μM DPI for 30 min and then exposed to 0.75 mM oxalate along with DPI for 3 h, after which PKC activity was measured. DMSO was used as a vehicle. Data are normalized to control, and values are expressed as means ± SE. Comparisons shown: a, significant compared with control; b, significant compared with DPI-treated control. *P < 0.05; n = 3.