J Korean Dent Soc Anesthesiol.
2014 Mar;14(1):41-47. 10.17245/jkdsa.2014.14.1.41.
The Effect of Propofol on Hypoxic damaged-HaCaT Cells
- Affiliations
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- 1Department of Dental Anesthesia and Pain Medicine, School of Dentistry, Pusan National University, Dental Research Institute, Busan, Korea. anekch@pusan.ac.kr
- 2Department of Oral Anatomy School of Dentistry, School of Dentistry, Pusan National University, Busan, Korea.
- 3Department of Oral and Maxillofacial Surgery, School of Dentistry, Pusan National University, Busan, Korea.
- 4Department of Anesthesia and Pain Medicine, School of Medicine, Pusan National University, Busan, Korea.
- KMID: 2345003
- DOI: http://doi.org/10.17245/jkdsa.2014.14.1.41
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℃ 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 µM) 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.
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