Fig. 5

Pharmacological blockade of G6PD abrogates the pro-inflammatory action by IL1β and its potentiation by glucose. (a) NADPH oxidase activity, determined by lucigenin-derived chemiluminescence in cells exposed to IL1β (10 ng/mL) after 18 h of incubation, in the presence or absence of 6-aminonicotinamide (6-ANAM; 2 mmol/L), in medium initially containing 5.5 or 22 mmol/L glucose. Results are the mean ± standard error of 3–6 separate experiments expressed as percentage of the relative light units produced by 10 ng/mL IL1β in medium initially containing 5.5 mmol/L glucose (380.1 ± 59.7 RLU/µg protein min⁻¹). (b) NFκB activation, measured by EMSA, and (c) iNOS levels, determined by Western blot, after 18 h exposure of cells to IL1β (10 ng/mL), in the presence or absence of 6-ANAM (2 mmol/L) in medium containing 5.5 or 22 mmol/L glucose. Results are the mean ± standard error of 3–5 separate experiments expressed as percentage of the activation or the expression produced by treatment with IL1β in medium containing 5.5 mmol/L glucose. *P < 0.05 vs respective control (c). ^† P < 0.05 vs respective value in 5.5 mmol/L glucose