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

Published online November 30, 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
Jul 31, 2022 Vol.45 No.7, pp. 435~512
COVER PICTURE
Mesenchymal stem cells (MSCs) are multipotent stem cells capable of differentiating into mesodermal lineages like adipogenic, osteogenic, and chondrogenic. Alcian blue-positive extracellular matrix secreted by chondrocytes in the lacuna confirmed the chondrogenic differentiation of MSCs (Bashyal et al., pp. 479-494).

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