Introduction: Acute kidney injury (AKI) is a clinical emergency caused by the rapid decline of renal function caused by various etiologies. Growth differentiation factor 11 (GDF11) can promote renal tubular regeneration and improve kidney function in AKI, but the specific mechanism remains unclear. Herein, we investigated the effect and mechanisms of GDF11 in ameliorating acute kidney injury (AKI) induced by ischemia-reperfusion (I/R). Methods: An animal model of acute kidney injury was established by I/R method, and the changes of serum urea nitrogen and creatinine were measured to evaluate the acute kidney injury. Enzyme-Linked Immunosorbent Assay (ELISA) was used to measure cytokines, malondialdehyde (MDA), superoxide dismutase (SOD), nitric oxide synthase (iNOS), and arginase 1 (Arg-1) levels. Flow cytometry was used to count the M1/M2 macrophages. IHC, WB, and q-PCR experiments were used to evaluate the expression of GDF11. Results: The changes in serum levels of urea nitrogen and creatinine after I/R suggest that an animal model of acute kidney injury (AKI) induced by I/R was successfully established. AKI caused by I/R significantly changed the M1/M2 macrophage polarization balance, with an increase in M2 being significantly higher than M1 an well as increased oxidative stress. Treatment with GDF11 after I/R significantly increased the differentiation of M2 cells and inhibited the differentiation of M1 macrophages, as well as decreased oxidative stress. Conclusion: GDF11 can promote the repair of acute kidney injury caused by ischemia-reperfusion by regulating the balance of M1/M2 polarization in macrophages and oxidative stress.

The Author(s). Published by S. Karger AG, Basel