The Effects Of Etomidate Preconditioning On The Change Of Mitochondrial Membrane Potential And The Opening Of The Mitochondrial Permeability Transition Pore In HL-60 Cells

Objective: Choose the apoptosis of HL-60 cells as the research object. Through the former study, the administration method of precondition may decrease the immunosuppressive effect of intravenous anesthetics, on the basis of which, the effects of etomidate preconditioning on the change of mitochondrial membrane potential and the opening of the mitochondrial permeability transition Pore in HL-60 Cells are further studied.Methods: HL-60 cells were cultured at a concentration of 1.5×10~5/ml. Three groups were processed in accordance to different methods. The control group was blank (0μM etomidate for 24h); the preconditioning group was precondictioned with 1μM etomidate for 1h, washed etomidate out and allowed to recover for 4h, and then treated with 500μM for 24h; the injury group was treated with 500μM etomidate for 24h. CCK-8 assay measured the cell viability and proliferation. Using the fluorescence probe of JC-1 to detect the change of mitochondrial membrane potential and the fluorescence probe of Calcein AM to detect the opening of the mitochondrial permeability transition Pore.Results: 1.In CCK-8 assay, etomidate inhibited HL-60 viability in preconditioning and injury groups, but the percentage of active cells increased by 55.57% in preconditioning group compared with that in the injury group. 2. In the detection of mitochondrial membrane potential by fluorescent JC-1, the depressed proportion of mitochondrial membrane potential was decreased by 25.34%. 3. In the detection of the mitochondrial permeability transition pore opening, the fluorescence intensity was increased by 28.69% in the preconditioning group compared with that of the control group, which indicated that the opening of the mitochondrial permeability transition pore in the precondition group was inhibited.Conclusions: Precondition at low concentration of etomidate can reduce and delay the decrease of the mitochondrial membrane potential, the mechanism of which may be relevant to the inhibition of the mitochondrial permeability transition pore.