Journal of The Korean Dental Society of Anesthesiology (대한치과마취과학회지)

The Korean Dental Society of Anesthsiology (대한치과마취과학회)
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Propofol Post-conditioning Protects against COS-7 Cells in Hypoxia/reoxygenation Injury by Induction of Intracellular Autophagy

  • Kwak, Jin-Won (Department of Dental Anesthesia and Pain Medicine, School of Dentistry, Pusan National University, Dental Research Institude) ;
  • Kim, Eok-Nyun (Department of Dental Anesthesia and Pain Medicine, School of Dentistry, Pusan National University, Dental Research Institude) ;
  • Park, Bong-Soo (Department of Oral Anatomy School of Dentistry, Pusan National University) ;
  • Kim, Yong-Ho (Department of Oral Anatomy School of Dentistry, Pusan National University) ;
  • Kim, Yong-Deok (Department of Oral and Maxillofacial Surgery School of Dentistry, Pusan National University) ;
  • Yoon, Ji-Uk (Department of Anesthesia and Pain Medicine School of Medicine, Pusan National University) ;
  • Kim, Cheul-Hong (Department of Dental Anesthesia and Pain Medicine, School of Dentistry, Pusan National University, Dental Research Institude) ;
  • Yoon, Ji-Young (Department of Dental Anesthesia and Pain Medicine, School of Dentistry, Pusan National University, Dental Research Institude)
  • Received : 2014.03.27
  • Accepted : 2014.04.02
  • Published : 2014.03.31
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Abstract

Background: Propofol (2.6-diisopropylphenol) is a widely used intravenous anesthetic agent for the induction and maintenance of anesthesia during surgeries and sedation for ICU patients. Propofol has a structural similarity to the endogenous antioxidant vitamin E and exhibits antioxidant activities.13) However, the mechanism of propofol on hypoxia/reoxygenation (H/R) injury has yet to be fully elucidated. We investigated how P-PostC influences the autophagy and cell death, a cellular damage occurring during the H/R injury. Methods: The groups were randomly divided into the following groups: Control: cells were incubated in normoxia (5% CO2, 21% O2, and 74% N2) without propofol treatment. H/R: cells were exposed to 24 h of hypoxia (5% CO2, 1% O2, and 94% N2) followed by 12 h of reoxygenation (5% CO2, 21% O2, and 74% N2). H/R + P-PostC: cells post-treated with propofol were exposed to 24 h of hypoxia followed by 12 h of reoxygenation. 3-MA + P-PostC: cells pretreated with 3-MA and post-treated propofol were exposed to 24 h of hypoxia followed by 12 h of reoxygenation Results: The results of our present study provides a new direction of research on mechanisms of propofol-mediated cytoprotection. There are three principal findings of these studies. First, the application of P-PostC at the onset of reoxygenation after hypoxia significantly increased COS-7 cell viability. Second, the cellular protective effect of P-PostC in H/R induced COS-7 cells was probably related to activation of intra-cellular autophagy. And third, the autophagy pathway inhibitor 3-MA blocked the protective effect of P-PostC on cell viability, suggesting a key role of autophagy in cellular protective effect of P-PostC. Conclusions: These data provided evidence that P-PostC reduced cell death in H/R model of COS-7 cells, which was in agreement with the protection by P-PostC demonstrated in isolated COS-7 cells exposed to H/R injury. Although the this study could not represent the protection by P-PostC in vivo, the data demonstrate another model in which endogenous mechanisms evoked by P-PostC protected the COS-7 cells exposed to H/R injury from cell death.

Keywords

References

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