Abstract
The 24p3/neutrophil gelatinase-associated lipocalin (NGAL) protein plays an important protective role in acute kidney injury (AKI), but the exact mechanism remains unclear. Therefore, we have made a preliminary exploration of its mechanism. The experimental group was formed by constructing and transfecting 24P3 overexpressed plasmid into renal tubular epithelial cells. Western Bolt was used to detect NGAL expression. Cell proliferation was detected by CCK8 kit, cell death was detected by Hoechst 33342 and PI kit, mitochondrial morphology was observed under light microscope, reactive oxygen species (ROS) content was detected by fluorescence probe, and iron level and glutathione peroxidase 4 (GPX4) activity were detected by kit. Furthermore, the mechanism of NGAL action was further demonstrated by adding ferrostein-1 (Fer-1), an ferroptosis inhibitor, and erastin (containing DMSO),an ferroptosis inductor. We found that ferroptosis-related indicators were lower in the NGAL overexpression group than in the control group. At the same time, we found that NGAL alleviated ferroptosis induced by erastin and coordinated with Fer-1 to alleviate ferroptosis. In conclusion, NGAL inhibits ferroptosis in renal tubular epithelial cells, which may be associated with the progression of AKI and may provide a new therapeutic target for the transition from acute kidney injury to chronic kidney injury.