Diabetic nephropathy (DN) is a common complication of diabetes mellitus and cell death is a key issue in DN. Ferroptosis is a recently discovered type of iron-dependent cell death and different from other kinds of cell death including apoptosis and necrosis. However, ferroptosis has not been described in the context of DN. This study was to explore the role of ferroptosis in the DN pathophysiology and to explore the efficacy of ferroptosis inhibitor SRS 16-86 on DN. The STZ injection was used to establish the DM and DN animal models. We detected the levels of iron, reactive oxygen species, and ferroptosis-specific markers in a rat DN model to investigate whether there was ferroptosis in the process of DN. The hematoxylin-eosin staining, blood biochemistry, urine biochemistry and the of function kidney were used to evaluate the efficacy of ferroptosis inhibitor-SRS 16-86 in repairing DN. We found that SRS 16-86 could improve the recovery of renal function after DN by improving the antiferroptosis factors glutathione peroxidase 4, glutathione, and system Xc-light chain and could lower the lipid peroxidation marker and 4-hydroxynonenal. SRS 16-86 treatment may improve the structure of renal organization after DN. Inflammatory cytokines-interleukin 1β and tumor necrosis factor α, and intercellular adhesion molecule 1 were decreased significantly following SRS 16-86 treatment after DN. Results indicate that there is a strong connection between ferroptosis and the pathological mechanism of DN. The validity of SRS 16-86, a ferroptosis inhibitor in DN repair, supports its potential as a new therapeutic target for DN.