Propofol protects against oxidative-stress-induced COS-7 cell apoptosis by inducing autophagy

BACKGROUND: In oxidative stress, reactive oxygen species (ROS) production contributes to cellular dysfunction and initiates the apoptotic cascade. Autophagy is considered the mechanism that decreases ROS concentration and oxidative damage. Propofol shows antioxidant properties, but the mechanisms underlying the effect of propofol preconditioning (PPC) on oxidative injury remain unclear. Therefore, we investigated whether PPC protects against cell damage from hydrogen peroxide (H(2)O(2))-induced oxidative stress and influences cellular autophagy. METHOD: COS-7 cells were randomly divided into the following groups: control, cells were incubated in normoxia (5% CO(2), 21% O(2), and 74% N(2)) for 24 h without propofol; H(2)O(2), cells were exposed to H(2)O(2) (400 µM) for 2 h; PPC + H(2)O(2), cells pretreated with propofol were exposed to H(2)O(2); and 3-methyladenine (3-MA) + PPC + H(2)O(2), cells pretreated with 3-MA (1 mM) for 1 h and propofol were exposed to H(2)O(2). Cell viability was determined using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide thiazolyl blue (MTT) reduction. Apoptosis was determined using Hoechst 33342 staining and fluorescence microscopy. The relationship between PPC and autophagy was detected using western blot analysis. RESULTS: Cell viability decreased more significantly in the H(2)O(2) group than in the control group, but it was improved by PPC (100 µM). Pretreatment with propofol effectively decreased H(2)O(2)-induced COS-7 cell apoptosis. However, pretreatment with 3-MA inhibited the protective effect of propofol during apoptosis. Western blot analysis showed that the level of autophagy-related proteins was higher in the PPC + H(2)O(2) group than that in the H(2)O(2) group. CONCLUSION: PPC has a protective effect on H(2)O(2)-induced COS-7 cell apoptosis, which is mediated by autophagy activation.