Journal of The Korean Dental Society of Anesthesiology (대한치과마취과학회지)

The Korean Dental Society of Anesthsiology (대한치과마취과학회)
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The Effect of Propofol on Hypoxic damaged-HaCaT Cells

  • Park, Chang-Hoon (Department of Dental Anesthesia and Pain Medicine, School of Dentistry, Pusan National University, Dental Research Institute) ;
  • Kwak, Jin-Won (Department of Dental Anesthesia and Pain Medicine, School of Dentistry, Pusan National University, Dental Research Institute) ;
  • 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) ;
  • Yoon, Ji-Young (Department of Dental Anesthesia and Pain Medicine, School of Dentistry, Pusan National University, Dental Research Institute) ;
  • Kim, Cheul-Hong (Department of Dental Anesthesia and Pain Medicine, School of Dentistry, Pusan National University, Dental Research Institute)
  • Received : 2014.03.26
  • Accepted : 2014.03.27
  • Published : 2014.03.31
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Abstract

Background: Autophagy is a self-eating process that is important for balancing sources of energy at critical times in development and in response stress. Autophagy also plays a protective role in removing clearing damaged intracellular organelles and aggregated proteins as well as eliminating intracellular pathogens. The purpose of the present study was to examine the protective effect of propofol against hypoxic damage using keratinocytes. Methods: Human keratinocytes (HaCaT cells) were obtained from the American Type Culture Collection. Propofol which were made by dissolving them in DMSO were kept frozen at $-4^{\circ}C$ until use. The stock was diluted to their concentration with DMEM when needed. Prior to propofol treatment cells were grown to about 80% confluence and then exposed to propofol at different concentrations (0, 25, 50, 75, $100{\mu}M$) for 2 h pretreatment. Cell viability was measured using a quantitative colorimetric assay with thiazolyl blue tetrazolium bromide (MTT assay), and fluorescence microscopy and western blot analysis were used for evaluation of autophagy processes. Results: The viability of propofol-treated HaCaT cells was increased in a dose-dependent manner. Propofol did not show any significant toxic effect on the HaCaT cells. The autophagy inhibitor, 3-methyladenine, reduced cell viability of hypoxia-injured HaCat cells. Fluorescence microscopy and western blot analysis showed propofol induce autophagy pathway signals. Conclusions: Propofol enhanced viability of hypoxia-injured HaCaT cells and we suggest propofol has cellular protective effects by autophagy signal pathway activation.

Keywords

References

  1. Martin P: Wound healing--aiming for perfect skin regeneration. Science 1997; 276(5309): 75-81. https://doi.org/10.1126/science.276.5309.75
  2. Buisson AC, Gilles C, Polette M, Zahm JM, Birembaut P, Tournier JM: Wound repair-induced expression of a stromelysins is associated with the acquisition of a mesenchymal phenotype in human respiratory epithelial cells. Lab Invest 1996; 74(3): 658-69.
  3. Laderoute KR, Webster KA: Hypoxia/reoxygenation stimulates Jun kinase activity through redox signaling in cardiac myocytes. Circ Res 1997; 80(3): 336-44. https://doi.org/10.1161/01.RES.80.3.336
  4. Nakatogawa H, Suzuki K, Kamada Y, Ohsumi Y: Dynamics and diversity in autophagy mechanisms: lessons from yeast. Nat Rev Mol Cell Biol 2009; 10(7): 458-67. https://doi.org/10.1038/nrm2708
  5. Levine B, Kroemer G: Autophagy in the pathogenesis of disease. Cell 2008; 132(1): 27-42. https://doi.org/10.1016/j.cell.2007.12.018
  6. Mizushima N: Autophagy: process and function. Genes Dev 2007; 21(22): 2861-73. https://doi.org/10.1101/gad.1599207
  7. Czaja MJ: Functions of autophagy in hepatic and pancreatic physiology and disease. Gastroenterology 2011; 140(7): 1895-908. https://doi.org/10.1053/j.gastro.2011.04.038
  8. Rautou PE, Mansouri A, Lebrec D, Durand F, Valla D, Moreau R: Autophagy in liver diseases. J Hepatol 2010; 53(6): 1123-34. https://doi.org/10.1016/j.jhep.2010.07.006
  9. Gulcin I, Alici HA, Cesur M: Determination of in vitro antioxidant and radical scavenging activities of propofol. Chem Pharm Bull (Tokyo) 2005; 53(3): 281-5. https://doi.org/10.1248/cpb.53.281
  10. Wang B, Shravah J, Luo H, Raedschelders K, Chen DD, Ansley DM: Propofol protects against hydrogen peroxideinduced injury in cardiac H9c2 cells via Akt activation and Bcl-2 up-regulation. Biochem Biophys Res Commun 2009; 389(1): 105-11. https://doi.org/10.1016/j.bbrc.2009.08.097
  11. Jin YC, Kim W, Ha YM, Shin IW, Sohn JT, Kim HJ, Seo HG, Lee JH, Chang KC: Propofol limits rat myocardial ischemia and reperfusion injury with an associated reduction in apoptotic cell death in vivo. Vascul Pharmacol 2009; 50(1-2): 71-7. https://doi.org/10.1016/j.vph.2008.10.002
  12. Kuma A, Hatano M, Matsui M, Yamamoto A, Nakaya H, Yoshimori T, Ohsumi Y, Tokuhisa T, Mizushima N: The role of autophagy during the early neonatal starvation period. Nature 2004; 432(7020): 1032-6. https://doi.org/10.1038/nature03029
  13. Scherz-Shouval R, Elazar Z: Regulation of autophagy by ROS: physiology and pathology. Trends Biochem Sci 2011; 36(1): 30-8. https://doi.org/10.1016/j.tibs.2010.07.007
  14. Huett A, Goel G, Xavier RJ: A systems biology viewpoint on autophagy in health and disease. Curr Opin Gastroenterol 2010; 26(4): 302-9. https://doi.org/10.1097/MOG.0b013e32833ae2ed
  15. Yin XM, Ding WX, Gao W: Autophagy in the liver. Hepatology 2008; 47(5): 1773-85. https://doi.org/10.1002/hep.22146
  16. Lu Z, Dono K, Gotoh K, Shibata M, Koike M, Marubashi S, Miyamoto A, Takeda Y, Nagano H, Umeshita K, Uchiyama Y, Monden M: Participation of autophagy in the degeneration process of rat hepatocytes after transplantation following prolonged cold preservation. Arch Histol Cytol 2005; 68(1): 71-80. https://doi.org/10.1679/aohc.68.71
  17. Loos B, Genade S, Ellis B, Lochner A, Engelbrecht AM: At the core of survival: autophagy delays the onset of both apoptotic and necrotic cell death in a model of ischemic cell injury. Exp Cell Res 2011; 317(10): 1437-53. https://doi.org/10.1016/j.yexcr.2011.03.011