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Fig. 4 | Cardiovascular Diabetology

Fig. 4

From: Inflammation, glucose, and vascular cell damage: the role of the pentose phosphate pathway

Fig. 4

High glucose medium potentiates the NADPH oxidase activation induced by IL1β. (a) Cells were exposed to IL1β (2.5 and 10 ng/mL), in the presence or absence of the IL1 receptor antagonist anakinra (1 µg/mL), in medium initially containing 5.5 or 22 mmol/L glucose. NADPH oxidase activity was determined by lucigenin-derived chemiluminescence after 18 h. Results are the mean ± standard error of 3–15 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 (472.7 ± 30.3 RLU/µg protein min−1). (b) NADPH oxidase activity in cells exposed to IL1β (10 ng/mL) or sodium azide (0.5 mmol/L) and in GLUT1- and EV-transfected cells after 18 h of incubation in medium initially containing 5.5 or 22 mmol/L glucose. Results are the mean ± standard error of 3–5 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 (457.1 ± 64.0 RLU/µg protein min−1). (c) NFκB activity, measured by EMSA, and (d) iNOS levels, determined by Western blot, in cells treated for 18 h with IL1β (10 ng/mL), in the presence or absence of the NADPH oxidase inhibitor apocynin (30 µmol/L) or anakinra (1 µg/mL), in medium containing 5.5 or 22 mmol/L glucose. Results are the mean ± standard error of 3–4 separate experiments expressed as percentage of the activation or expression produced by 10 ng/mL IL1β in medium initially 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

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