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논문 기본 정보

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저자정보
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)
저널정보
대한치과마취과학회 Journal of dental anesthesia and pain medicine Journal of dental anesthesia and pain medicine 제14권 제1호
발행연도
2014.1
수록면
49 - 56 (8page)

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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.
#Cos-7 cells #Hypoxia reoxygenation #Post-Treated #Propofol

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Anderson RT / 2004 / Development and validation of the insulin treatment satisfaction questionnaire / Clin Ther 26(4):565~578 google schola Hamacher-Brady A / 2006 / Enhancing macroautophagy protects against ischemia/reperfusion injury in cardiac myocytes / J Biol Chem 281(40):29776~29787 google schola Kuma A / 2004 / The role of autophagy during the early neonatal starvation period / Nature 432(7020):1032~1036 google schola Hamacher-Brady A / 2007 / Response to myocardial ischemia/reperfusion injury involves Bnip3and autophagy / Cell Death Differ 14(1):146~157 google schola Murry CE / 1986 / Preconditioning with ischemia: a delay of lethal cell injury in ischemic myocardium / Circulation 74(5):1124~1136 google schola

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