Related Experiment Video
Updated: Jun 17, 2025
Author Spotlight: Improved Localization and Monitoring of Coronary Flow Reserve Using Modified PLAX View in Mice
Published on: August 25, 2023
Sevoflurane Affects Myocardial Autophagy Levels After Myocardial Ischemia Reperfusion Injury via the
Jiying Ao1, Xueting Zhang1, Degang Zhu2
1Department of Anesthesiology, Wuhan No.1 Hospital, 215 Zhongshan Dadao, Wuhan, 430030, Hubei, China.
Abstract:
This research focused on investigating the effects of sevoflurane (Sev) on myocardial autophagy levels after myocardial ischemia reperfusion (I/R) injury via the microRNA-542-3p (miR-542-3p)/ADAM9 axis. Mice underwent 30 min occlusion of the left anterior descending coronary (LAD) followed by 2 h reperfusion. Cardiac infarction was determined by 2,3,5-triphenyltetrazolium chloride triazole (TTC) staining. Cardiac function was examined by echocardiography. Cardiac markers and oxidative stress factors were evaluated by ELISA. Autophagy-associated factors were detected by western blot. Relationship between miR-542-3p and ADAM9 was tested by dual-luciferase reporter gene assay, RT-qPCR, and western blot. Sev treatment ameliorated cardiac dysfunction, myocardial oxidative stress, and histopathological damages, decreased myocardial infarction size and myocardial apoptotic cells after myocardial I/R injury. Sev treatment elevated miR-542-3p expression and decreased ADAM9 expression in myocardial tissues after myocardial I/R injury. miR-542-3p overexpression could enhance the ameliorative effects of Sev on myocardial injury and myocardial autophagy in I/R mice. miR-542-3p targeted and negatively regulated ADAM9 expression. ADAM9 overexpression reversed the ameliorative effects of miR-542-3p up-regulation on myocardial injury and myocardial autophagy in Sev-treated I/R mice. Sev treatment could ameliorate myocardial injury and myocardial autophagy in I/R mice, mediated by mechanisms that include miR-542-3p up-regulation and ADAM9 down-regulation.
Insights
Sevoflurane (Sev) protects against myocardial ischemia reperfusion (I/R) injury by upregulating microRNA-542-3p (miR-542-3p) and downregulating ADAM9, thereby improving cardiac function and reducing autophagy.
Area of Science:
- Cardiology
- Molecular Biology
- Pharmacology
Background:
- Myocardial ischemia reperfusion (I/R) injury is a significant clinical concern.
- Autophagy plays a complex role in I/R injury.
- The microRNA-542-3p (miR-542-3p)/ADAM9 axis is implicated in cardiac injury.
Purpose of the Study:
- To investigate the protective effects of sevoflurane (Sev) on myocardial I/R injury.
- To elucidate the role of the miR-542-3p/ADAM9 axis in Sev-mediated cardioprotection.
- To examine the impact of Sev on myocardial autophagy.
Main Methods:
- Mice underwent surgical induction of myocardial I/R.
- Sevoflurane treatment was administered.
- Cardiac function, infarction size, oxidative stress, and autophagy markers were assessed.
- miR-542-3p and ADAM9 expression levels were quantified.
- Dual-luciferase reporter assays and molecular interventions were employed.
Main Results:
- Sevoflurane treatment reduced myocardial infarction size, improved cardiac function, and decreased oxidative stress and apoptosis.
- Sev increased miR-542-3p expression and decreased ADAM9 expression in I/R hearts.
- miR-542-3p targeted and negatively regulated ADAM9.
- Overexpression of miR-542-3p enhanced Sev's protective effects, while ADAM9 overexpression reversed them.
Conclusions:
- Sevoflurane exerts protective effects against myocardial I/R injury.
- These effects are mediated, at least in part, by the upregulation of miR-542-3p and the subsequent downregulation of ADAM9.
- The miR-542-3p/ADAM9 axis is a key pathway involved in Sev-induced cardioprotection and modulation of myocardial autophagy.
