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KMID : 0980320170170010021
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Journal of Dental Anesthesia and Pain Medicine
2017 Volume.17 No. 1 p.21 ~ p.28
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Propofol protects human keratinocytes from oxidative stress via autophagy expression
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Yoon Ji-Young
Jeon Hyun-Ook
Kim Eun-Jung
Kim Cheul-Hong
Yoon Ji-Uk
Park Bong-Soo
Yu Su-Bin
Kwak Jin-Won
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Abstract
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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% CO2, 21% O2, and 74% N2) without propofol; hydrogen peroxide (H2O2), cells were exposed to H2O2 (300 μM) for 2 h; propofol preconditioning (PPC)/H2O2, cells pretreated with propofol (100 μM) for 2 h were exposed to H2O2; and 3-methyladenine (3-MA)/PPC/H2O2, cells pretreated with 3-MA (1 mM) for 1 h and propofol were exposed to H2O2. Cell viability, apoptosis, and migration capability were evaluated. Relation to autophagy was detected by western blot analysis.
Results: Cell viability decreased significantly in the H2O2 group compared to that in the control group and was improved by propofol preconditioning. Propofol preconditioning effectively decreased H2O2-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/H2O2 group compared to that in the H2O2 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.
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KEYWORD
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Keratinocytes, Oxidative Stress, Propofol
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