RETRACTED: Effects of propofol on cardiac function and miR-494 expression in rats with hepatic ischemia/reperfusion injury
Objective This study aimed to investigate the effects of propofol on cardiac function and miR-494 expression in rats with hepatic ischemia/reperfusion (I/R) injury. Methods Forty healthy adult male Sprague-Dawley rats were allocated to the sham operation group and three hepatic I/R injury groups. Th...
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Published in: | Journal of international medical research Vol. 49; no. 3 |
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Main Authors: | , , , , |
Format: | Journal Article |
Language: | English |
Published: |
London, England
SAGE Publications
01-03-2021
Sage Publications Ltd SAGE Publishing |
Online Access: | Get full text |
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Summary: | Objective This study aimed to investigate the effects of propofol on cardiac function and miR-494 expression in rats with hepatic ischemia/reperfusion (I/R) injury. Methods Forty healthy adult male Sprague-Dawley rats were allocated to the sham operation group and three hepatic I/R injury groups. The I/R injury groups included I/R injury only (I/R group), treatment with propofol (propofol group), and treatment with propofol + overexpressed miR-494 (propofol+miR-494 group). Apoptosis of myocardial cells and changes in cardiac function indices, including left ventricular end-diastolic diameter, left ventricular end-systolic diameter, and left ventricular posterior wall thickness, as well as changes in miR-494, were monitored. Results The apoptotic rate of myocardial cells in the I/R group was higher, cardiac function was deteriorated, and miR-494 levels were elevated compared with the sham group. The apoptotic rate was lower, cardiac function was improved, and miR-494 levels were suppressed in the propofol group compared with the I/R group. The apoptotic rate was higher, cardiac function was deteriorated, and miR-494 levels were elevated in the propofol+miR-494 group compared with the propofol group. Conclusion Propofol plays a vital role in preventing myocardial cell apoptosis and improvement of cardiac function by suppressing miR-494 in a hepatic I/R injury rat model. |
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ISSN: | 0300-0605 1473-2300 |
DOI: | 10.1177/0300060521990988 |