Aim
To explore the function of circ_UTRN in acute pancreatitis (AP).
Conclusion
circ_UTRN inhibited oxidative stress and ferroptosis by regulating the miR-760-3p/FOXO1/GPX4 axis. This is a potential new treatment strategy for AP.
Methods
After exposing AR42J cells to caerulein, the levels of circ_UTRN, miR-760-3p, and glutathione peroxidase 4 (GPX4) were determined by quantitative polymerase chain reaction. Additionally, GPX4 and forkhead box O1 (FOXO1) protein levels were assessed by western blot. The levels of oxidative stress and ferroptosis in the supernatant of the treated AR42J cells were also assessed using commercial kits.
Results
circ_UTRN inhibited caerulein-induced oxidative stress and ferroptosis by binding with miR-760-3p. Additionally, miR-760-3p directly targeted FOXO1, thereby regulating GPX4 levels. Furthermore, GPX4 knockdown abolished the effect of miR-760-3p downregulation in AP.