Propofol postconditioning protects H9c2 cells from hypoxia/reoxygenation injury by inducing autophagy via the SAPK/JNK pathway

Propofol postconditioning (P-PostC) offers cardioprotection in mice, and the upregulation of autophagy protects cardiac cells against ischemia/reperfusion injury. The present study aimed to examine the effects of P-PostC on the induction of autophagy and its potential roles in hypoxia/reoxygenation...

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Bibliographic Details
Published in:Molecular medicine reports Vol. 17; no. 3; pp. 4573 - 4580
Main Authors: Li, Hao, Zhang, Xuan, Tan, Jian, Sun, Li, Xu, Long-He, Jiang, Yu-Ge, Lou, Jing-Sheng, Shi, Xue-Yin, Mi, Wei-Dong
Format: Journal Article
Language:English
Published: Greece D.A. Spandidos 01.03.2018
Spandidos Publications
Spandidos Publications UK Ltd
Subjects:
Adenine - analogs & derivatives
Adenine - pharmacology
Animals
Anthracenes - pharmacology
Apoptosis
Autophagy
Autophagy - drug effects
Biotechnology
c-Jun protein
Cardiomyocytes
cardioprotection
Cell culture
Cell Hypoxia
Cell survival
Dosage and administration
Drug interactions
Health aspects
Heart
Heart diseases
Hypoxia
Immunofluorescence
Ischemia
ischemic postconditioning
JNK Mitogen-Activated Protein Kinases - antagonists & inhibitors
JNK Mitogen-Activated Protein Kinases - metabolism
JNK protein
Kinases
L-Lactate dehydrogenase
L-Lactate Dehydrogenase - metabolism
Lactic acid
MAP kinase
MAP Kinase Signaling System - drug effects
Microtubule-Associated Proteins - metabolism
myocardial ischemia
Myocytes
Myocytes, Cardiac - cytology
Myocytes, Cardiac - metabolism
Observations
Oxygen - pharmacology
Phagocytosis
Phosphorylation
Phosphorylation - drug effects
Propofol
Propofol - pharmacology
Protein kinases
Proteins
Rats
Reperfusion
Sequestosome-1 Protein - metabolism
Stem cells
Studies
Transcription factors
Transmission electron microscopy
Western blotting
United States > US
ISSN:1791-2997, 1791-3004, 1791-3004
Online Access:Get full text
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Summary:Propofol postconditioning (P-PostC) offers cardioprotection in mice, and the upregulation of autophagy protects cardiac cells against ischemia/reperfusion injury. The present study aimed to examine the effects of P-PostC on the induction of autophagy and its potential roles in hypoxia/reoxygenation (H/R) injury. Rat heart-derived H9c2 cells were exposed to H/R, comprising 6 h of hypoxia followed by 4 h of reoxygenation, as well as postconditioning with various concentrations of propofol at the onset of reperfusion. Lactate dehydrogenase (LDH) activity and the rate of cell apoptosis were measured to evaluate the degree of cardiomyocyte H/R injury. The induction of autophagy in myocytes subjected to H/R injury and P-PostC was detected by western blotting and immunofluorescence. Furthermore, the activation of c-Jun N-terminal kinase (JNK) in cells treated with P-PostC with or without co-treatment with SP600125, an inhibitor of JNK, was also determined by western blotting. P-PostC reduced the activity of LDH in the culture medium and the percentage of apoptotic cells compared with cells in the untreated H/R group. In addition, P-PostC induced autophagy and promoted survival signaling in H9c2 cardiac myoblast cells. The inhibition of autophagy by 3-methyladenine treatment diminished the cardioprotective effects of P-PostC. These results indicated that propofol postconditioning promoted cell survival through the induction of autophagy in H9c2 cardiac cells, and that the stress-activated protein kinase/JNK survival pathway may be partly involved in P-PostC-induced autophagy.
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ISSN:1791-2997
1791-3004
1791-3004
DOI:10.3892/mmr.2018.8424