Propofol protects human keratinocytes from oxidative stress via autophagy expression.
10.17245/jdapm.2017.17.1.21
- Author:
Ji Young YOON
1
;
Hyun Ook JEON
;
Eun Jung KIM
;
Cheul Hong KIM
;
Ji Uk YOON
;
Bong Soo PARK
;
Su Bin YU
;
Jin Won KWAK
Author Information
1. Department of Dental Anesthesia and Pain Medicine, School of Dentistry, Pusan National University, Dental Research Institute, Yangsan, Republic of Korea. dentiwon@hanmail.net
- Publication Type:Original Article
- Keywords:
Keratinocytes;
Oxidative Stress;
Propofol
- MeSH:
Apoptosis;
Autophagy*;
Blotting, Western;
Cell Death;
Cell Movement;
Cell Survival;
Humans*;
Hydrogen Peroxide;
Keratinocytes*;
Methods;
Oxidative Stress*;
Propofol*;
Reactive Oxygen Species;
Skin;
Water
- From:Journal of Dental Anesthesia and Pain Medicine
2017;17(1):21-28
- CountryRepublic of Korea
- Language:English
-
Abstract:
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.
