Desflurane restrains renal ischemia–reperfusion-stimulated endoplasmic reticulum stress and apoptosis via elevating microRNA-181c-5p to target DNA damage-inducible transcript 4

Renal ischemia/reperfusion injury (RI/RI) is the crucial cause of acute kidney injury.

The study was to explore the action mechanism of desflurane (DFE) pretreatment on RI/RI in rats. The RI/RI model of rats was constructed, and serum renal function parameters (blood urea nitrogen and serum creatinine) were detected adopting corresponding commercial kits to assess renal function injury. Detection of renal tissue damage was performed. Test of cell apoptosis was implemented. Examination of endoplasmic reticulum stress (ERS)-associated proteins C/EBP homologous protein, glucose regulatory protein 78, and activation transcription factor 6 was performed. Test of concentrations of interleukin-1β and tumor necrosis factor-αwas implemented.

The results illustrated DFE restrained renal ischemia–reperfusion (RIR)-stimulated ERS and apoptosis, and DFE elevated miR-181c-5p and suppressed DDIT4 inRIR rats. MicroRNA (miR)-181c-5p was declined in RIR rats and ameliorated ischemia–reperfusion-stimulated ERS and apoptosis, suppressive miR-181c-5p or elevated DDIT4 turned around the protection of DFE on RIR. MiR-181c-5p targeted DNA damage-inducible transcript 4 (DDIT4).

The study offered theoretical foundation for further exploration on DFE in repressing RIR-stimulated ERS and apoptosis via elevating miR-181c-5p to target DDIT4.