Background: Cardiopulmonary bypass (CPB) caused postoperative cognitive dysfunction
(POCD) was characterized by hippocampus apoptosis, which seriously limited the therapeutic
efficacy and utilization of CPB in clinic. Recent data indicated that sevoflurane anesthesia might
alleviate CPB-induced POCD, however, the underlying mechanisms are still unclear.
Methods: In the present study, the in vivo CPB-POCD models were established by using aged
Sprague-Dawley (SD) male rats and the in vitro hypoxia/reoxygenation (H/R) models were inducted
by using the primary hippocampus neuron (PHN) cells.
Results: The results showed that CPB impaired cognitive functions and induced hippocampus
apoptosis in rat models, which were alleviated by pre-treating rats with low-dose sevoflurane. In
addition, the phosphatidylinositol 3 kinase (PI3K)/protein kinase B (AKT) signal pathway was inactivated
in the hippocampus tissues of CPB-POCD rats, which were rescued by low-dose sevoflurane
treatment. Of note, the PI3K/AKT inhibitor (LY294002) abrogated the protective effects of
low-dose sevoflurane on CPB-POCD rats. Consistently, the in vitro results showed that H/R treatment
induced cell apoptosis and inhibited cell viability in PHN cells, which were attenuated by
low-dose sevoflurane. Similarly, LY294002 abrogated the inhibiting effects of low-dose sevoflurane
on H/R-induced PHN cell death.
Conclusion: Taken together, low-dose sevoflurane attenuated CPB-induced POCD by inhibiting
hippocampus apoptosis through activating PI3K/AKT signal pathway.