Exogenous pentraxin-3 inhibits the reactive oxygen species-mitochondrial and apoptosis pathway in acute kidney injury

Abstract

Purpose: Pextraxin-3 (PTX3) is a long pentraxin group and has been studied for inflammatory diseases and various organs. We found that PTX3 has a positive effect on PTX3 in proliferating kidney cell proliferation during ischemia and proinflammatory acute kidney injury (AKI). The aim of this study was to develop an experimental model of AKI in vitro and to analyze the protective mechanism of exogenous recombinant PTX3. Materials and Methods: We used HK-2 which was a renal tubular cell line. Calcium ionophores (A23187) induced injury by increasing intracellular calcium concentration and exogenous recombinant PTX3, was treated on the injured cells. Also, we confirmed the expression of caspase-3 and PARP which are involved in intracellular ROS and apoptosis. Results: Fluorescence microscopy revealed a significant increase in the influx of intracellular calcium due to A23187, resulting in renal cell damage, and increased calpain activity. After that, the activity of ROS rapidly increased after treatment with A23187 and decreased after treatment with exogenous recombinant PTX3. The activity of caspase-3 and PARP decreased after treatment with exogenous recombinant PTX3. Conclusion: PTX3 reduces ROS and calpain activity and stabilizes mitochondrial membrane potential. Also, PTX3 reduces apoptosis by decreasing caspase-3 and PARP. As a result, PTX3 blocks ROS, Calpain activity, mitochondria and apoptosis pathway, and consequently protects renal tubular cells.