Propofol protects human keratinocytes from oxidative stress via autophagy expression

BACKGROUND: The skin consists of tightly connected keratinocytes, and prevents extensive water loss while simultaneously protecting against the entry of microbial pathogens. Excessive cellular levels of reactive oxygen species can induce cell apoptosis and also damage skin integrity. Propofol (2,6-diisopropylphenol) has antioxidant properties. In this study, we investigated how propofol influences intracellular autophagy and apoptotic cell death induced by oxidative stress in human keratinocytes. METHOD: The following groups were used for experimentation: control, cells were incubated under normoxia (5% CO(2), 21% O(2), and 74% N(2)) without propofol; hydrogen peroxide (H(2)O(2)), cells were exposed to H(2)O(2) (300 µM) for 2 h; propofol preconditioning (PPC)/H(2)O(2), cells pretreated with propofol (100 µM) for 2 h 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, apoptosis, and migration capability were evaluated. Relation to autophagy was detected by western blot analysis. RESULTS: Cell viability decreased significantly in the H(2)O(2) group compared to that in the control group and was improved by propofol preconditioning. Propofol preconditioning effectively decreased H(2)O(2)-induced cell apoptosis and increased cell migration. However, pretreatment with 3-MA inhibited the protective effect of propofol on cell apoptosis. Autophagy was activated in the PPC/H(2)O(2) group compared to that in the H(2)O(2) group as demonstrated by western blot analysis and autophagosome staining. CONCLUSION: The results suggest that propofol preconditioning induces an endogenous cellular protective effect in human keratinocytes against oxidative stress through the activation of signaling pathways related to autophagy.