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Mol. Cells 2010; 30(5): 455-460

Published online September 2, 2010

https://doi.org/10.1007/s10059-010-0130-z

© The Korean Society for Molecular and Cellular Biology

Propofol Protects the Autophagic Cell Death Induced by the Ischemia/Reperfusion Injury in Rats

Hae Sook Noh, Il Woo Shin1, Ji Hye Ha, Young-Sool Hah2, Seon Mi Baek, and Deok Ryong Kim*

Department of Biochemistry, Gyeongsang National University School of Medicine, Jinju 660-751, Korea, 1Anesthesiology and Pain Medicine, Institute of Health Sciences, Gyeongsang National University School of Medicine, Jinju 660-751, Korea, 2Clinical Research Institute of Gyeongsang National University, Jinju 660-751, Korea

Correspondence to : *Correspondence: drkim@gsnu.ac.kr

Received: June 1, 2010; Revised: July 20, 2010; Accepted: July 29, 2010

Abstract

Autophagy has been implicated in cardiac cell death dur-ing ischemia/reperfusion (I/R). In this study we investi-gated how propofol, an antioxidant widely used for anes-thesia, affects the autophagic cell death induced by the myocardial I/R injury. The infarction size in the myocar-dium was dramatically reduced in rats treated with propofol during I/R compared with untreated rats. A large number of autophagic vacuoles were observed in the cardiomyocytes of I/R-injured rats but rarely in I/R-injured rats treated with propofol. While LC3-II formation, an autophagy marker, was up-regulated in the I/R-injured myocardium, it was significantly down-regulated in the myocardial tissues of I/R-injured and propofol-treated rats. Moreover, propofol inhibited the I/R-induced expression of Beclin-1, and it accelerated phosphorylation of mTOR during I/R and Beclin-1/Bcl-2 interaction in cells, which indicates that it facilitates the inhibitory pathway of autophagy. These data suggest that propofol protects the autophagic cell death induced by the myocardial I/R injury.

Keywords autophagy, Beclin-1/Bcl-2 interaction, cell death, ischemia/reperfusion, propofol

Article

Research Article

Mol. Cells 2010; 30(5): 455-460

Published online November 30, 2010 https://doi.org/10.1007/s10059-010-0130-z

Copyright © The Korean Society for Molecular and Cellular Biology.

Propofol Protects the Autophagic Cell Death Induced by the Ischemia/Reperfusion Injury in Rats

Hae Sook Noh, Il Woo Shin1, Ji Hye Ha, Young-Sool Hah2, Seon Mi Baek, and Deok Ryong Kim*

Department of Biochemistry, Gyeongsang National University School of Medicine, Jinju 660-751, Korea, 1Anesthesiology and Pain Medicine, Institute of Health Sciences, Gyeongsang National University School of Medicine, Jinju 660-751, Korea, 2Clinical Research Institute of Gyeongsang National University, Jinju 660-751, Korea

Correspondence to:*Correspondence: drkim@gsnu.ac.kr

Received: June 1, 2010; Revised: July 20, 2010; Accepted: July 29, 2010

Abstract

Autophagy has been implicated in cardiac cell death dur-ing ischemia/reperfusion (I/R). In this study we investi-gated how propofol, an antioxidant widely used for anes-thesia, affects the autophagic cell death induced by the myocardial I/R injury. The infarction size in the myocar-dium was dramatically reduced in rats treated with propofol during I/R compared with untreated rats. A large number of autophagic vacuoles were observed in the cardiomyocytes of I/R-injured rats but rarely in I/R-injured rats treated with propofol. While LC3-II formation, an autophagy marker, was up-regulated in the I/R-injured myocardium, it was significantly down-regulated in the myocardial tissues of I/R-injured and propofol-treated rats. Moreover, propofol inhibited the I/R-induced expression of Beclin-1, and it accelerated phosphorylation of mTOR during I/R and Beclin-1/Bcl-2 interaction in cells, which indicates that it facilitates the inhibitory pathway of autophagy. These data suggest that propofol protects the autophagic cell death induced by the myocardial I/R injury.

Keywords: autophagy, Beclin-1/Bcl-2 interaction, cell death, ischemia/reperfusion, propofol

Mol. Cells
Feb 28, 2023 Vol.46 No.2, pp. 69~129
COVER PICTURE
The bulk tissue is a heterogeneous mixture of various cell types, which is depicted as a skein of intertwined threads with diverse colors each of which represents a unique cell type. Single-cell omics analysis untangles efficiently the skein according to the color by providing information of molecules at individual cells and interpretation of such information based on different cell types. The molecules that can be profiled at the individual cell by single-cell omics analysis includes DNA (bottom middle), RNA (bottom right), and protein (bottom left). This special issue reviews single-cell technologies and computational methods that have been developed for the single-cell omics analysis and how they have been applied to improve our understanding of the underlying mechanisms of biological and pathological phenomena at the single-cell level.

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