NADPH Oxidase-Induced NALP3 Inflammasome Activation Is Driven by Thioredoxin-Interacting Protein Which Contributes to Podocyte Injury in Hyperglycemia

Figure 4

Inhibition of NADPH oxidase attenuates HG-induced NALP3 inflammasome activation and function. (a) Western blot analysis showing the expression of , NALP3, active caspase-1, and active IL-1β in HG-stimulated podocytes without or with shRNA transfection. (b) Summarized data showing the band intensities measured from , NALP3, active caspase-1, and active IL-1β (). (c) Immunoblotting presenting the expression of NALP3, active caspase-1, and active IL-1β in HG-stimulated podocytes without or with treatment of APO or DPI. (d) Summarized data showing the band intensities of NALP3, active caspase-1, and active IL-1β ( = 4–8). (e) Caspase-1 activity in podocytes treated with HG in the presence of various genetic and pharmacologic inhibition of NADPH oxidase (). (f) IL-1β concentration in the supernatant of podocytes treated with HG in the presence of various genetic and pharmacologic inhibitors of NADPH oxidase (). Ctrl: control; HG: high glucose; Veh: vehicle; Scram: scrambled shRNA; shgp91: shRNA; APO: apocynin; DPI: diphenyleneiodonium. compared with Ctrl. compared with HG group treated with vehicle or transfected with scramble shRNA.

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