RRM2 attenuates the renal tubular ferroptosis in diabetic kidney disease through PI3K/Akt/Nrf2 pathway

Figure 4 Ribonucleotide reductase regulatory subunit M2 overexpression suppresses cellular reactive oxygen species production and oxidative stress in high glucose-treated renal tubular cells via the PI3K/Akt signaling pathway. A: Representative images of dihydroergotamine (DHE) staining of HK-2 cells; B: Quantification of DHE-positive cells relative to DAPI-positive cells in the different groups; C-E: The colorimetric method was applied to analyze oxidative stress indicators in the lysate of HK-2 cells, and the levels of malondialdehyde (C), superoxide dismutase (D), and catalase (E) were measured. Data are presented as mean ± SD in triplicate and analyzed using one-way ANOVA. ^aP < 0.001 vs control group; ^bP < 0.001 vs high glucose (HG) group; ^cP < 0.001 vs HG + OE-ribonucleotide reductase regulatory subunit M2 group. HG: High glucose; OE-RRM2: Overexpressing ribonucleotide reductase regulatory subunit M2; DHE: Dihydroergotamine; MDA: Malondialdehyde; SOD: Superoxide dismutase; CAT: Catalase.