Corilagin alleviates podocyte injury in diabetic nephropathy by regulating autophagy via the SIRT1-AMPK pathway

Figure 7 Corilagin suppresses cellular reactive oxygen species production and oxidative stress in hyperglycemia-induced podocytes via SIRT1. MPC5 cells were pretreated with a SIRT1 inhibitor (EX-527, 10 μM) for 2 h, and then incubated with corilagin (50 μM) and high glucose (D-glucose 30 mM) for a further 48 h. A: Representative images of 2,7-dichlorodihydrofluorescein diacetate (DCFH-DA) staining of MPC5 cells; B: Quantification of DCFH-DA positive cells relative to DAPI positive cells; C-E: The colourimetric method was applied to analyze oxidative stress indicators in the lysate of MPC5 cells, and the levels of malondialdehyde, superoxide dismutase, and catalase were quantified. Data are presented as the mean ± SD (n = 8 in each group). ^aP < 0.001 vs control group; ^bP < 0.001 vs HG group; ^cP < 0.001 vs HG + Cor group. HG: High glucose; Cor: Corilagin; DN: Diabetic nephropathy; MDA: Malondialdehyde; SOD: Superoxide dismutase; CAT: Catalase.