Propofol Post-conditioning Protects against COS-7 Cells in Hypoxia/reoxygenation Injury by Induction of Intracellular Autophagy
´ëÇÑÄ¡°ú¸¶Ãë°úÇÐȸÁö 2014³â 14±Ç 1È£ p.49 ~ p.56
°ûÁø¿ø(Kwak Jin-Won) - Pusan National University School of Dentistry Department of Dental Anesthesia and Pain Medicine
(Kim Eok-Nyun) - Pusan National University School of Dentistry Department of Dental Anesthesia and Pain Medicine
¹ÚºÀ¼ö(Park Bong-Soo) - Pusan National University School of Dentistry Department of Oral Anatomy
±è¿µÈ£(Kim Yong-Ho) - Pusan National University School of Dentistry Department of Oral Anatomy
±è¿ë´ö(Kim Yong-Deok) - Pusan National University School of Dentistry Department of Oral and Maxillofacial Surgery
À±Áö¿í(Yoon Ji-Uk) - Pusan National University School of Medicine Department of Anesthesiology and Pain Medicine
±èöȫ(Kim Cheul-Hong) - Pusan National University School of Medicine Department of Anesthesiology and Pain Medicine
À±Áö¿µ(Yoon Ji-Young) - Pusan National University School of Dentistry Department of Dental Anesthesia and Pain Medicine
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.
Å°¿öµå
Cos-7 cells, Hypoxia reoxygenation, Post-Treated, Propofol
KMID :
0980220140140010049
¿ø¹® ¹× ¸µÅ©¾Æ¿ô Á¤º¸
µîÀçÀú³Î Á¤º¸
À¯È¿¼º°á°ú(Recomendation)