Sevoflurane reduces cerebral injuries in rats resuscitated from cardiac arrest through down-regulating the expression of Bax and Bak

Abstract

Objective To investigate the neuroprotective mechanism of sevoflurane in rats resuscitated from cardiac arrest (CA). Methods A ventricular fibrillation-induced CA model was established. Forty Wistar rats were randomly divided into the sham group, sevoflurane group and control group. Apoptosis-related proteins were measured by Western blot at 24 h after restoration of spontaneous circulation (ROSC). The status of mitochondrial permeability transition pore (MPTP) were measured using a spectrophotometer, and the mitochondrial membrane potential (MMP) were measured with JC-1 fluorescent probe. At 72 h after ROSC, the apoptotic index of neurons in hippocampal CA1 region was counted by TUNEL staining. Results The protein expression of Bax, Bak, cleaved-caspase 9, cleaved-caspase 3 and cytosolic cytochrome c were lower in the sevoflurane group (all P<0.05), the protein expression of Bcl-2 was higher in the sevoflurane group compared with the control group (P<0.05). The sevoflurane group had a less opening status of MPTP and a higher MMP compared with the control group (all P<0.05). The sevoflurane group had less apoptotic neurons compared with the control group (P<0.05). Conclusion By up-regulating the expression of Bcl-2, down-regulating Bax and Bak, sevoflurane could reduce the apoptosis of neurons and decrease the opening of MPTP, eventually reduce cerebral injuries. Key words: Cardiac arrest; Sevoflurane; Apoptosis; Mitochondrial permeability transition pore; Bax; Bak