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Protective Effect of Isoflurane on Hypoxia/Reoxygenation-Induced Myocardial Injury via miR-548a-5p Regulation of PTEN
Ji Yao1, Jianyong Zheng2, Wei Wei3
1Anesthesia Department, The Third People's Hospital Health Care Group of Cixi, Cixi, Zhejiang, China.
Abstract:
Ischemia-reperfusion (I/R) injury induces cardiomyocyte apoptosis, oxidative stress and elevated myocardial injury markers. This study aimed to investigate whether the microRNA-548a-5p (miR-548a-5p)/phosphatase and tensin homolog deleted on chromosome 10 (PTEN) axis mediates the cardioprotection conferred by isoflurane (ISO). An in vitro hypoxia/reoxygenation (H/R) injury model was established using H9c2 cardiomyocytes, including control, H/R and ISO pretreatment groups. We detected miR-548a-5p and PTEN expression by RT-qPCR, and evaluated cell viability, apoptosis, myocardial injury markers including creatine kinase-MB (CK-MB), cardiac troponin I (cTnI), lactate dehydrogenase (LDH), and reactive oxygen species (ROS) using CCK-8, flow cytometry, ELISA and DCFH-DA staining. Dual-luciferase reporter assay validated the direct binding between miR-548a-5p and PTEN. H/R downregulated miR-548a-5p and upregulated PTEN, accompanied by decreased cell viability, increased apoptosis, myocardial injury and oxidative stress. 1.0% ISO pretreatment reversed these adverse alterations, restored miR-548a-5p and suppressed PTEN expression. miR-548a-5p inhibition attenuated ISO-elicited cardioprotection, whereas PTEN silencing restored the cardioprotective capacity compromised by miR-548a-5p inhibition. In conclusion, ISO exerts cardioprotective effects via the miR-548a-5p/PTEN signaling axis, offering a potential therapeutic target for I/R injury.
Insights
Isoflurane protects heart cells from injury by regulating microRNA-548a-5p (miR-548a-5p) and phosphatase and tensin homolog deleted on chromosome 10 (PTEN). This miR-548a-5p/PTEN pathway offers a new therapeutic target for ischemia-reperfusion injury.
Area of Science:
- Cardiology
- Molecular Biology
- Anesthesiology
Background:
- Ischemia-reperfusion (I/R) injury causes cardiomyocyte apoptosis, oxidative stress, and elevated myocardial injury markers.
- Understanding the molecular mechanisms underlying I/R injury is crucial for developing effective treatments.
Purpose of the Study:
- To investigate if the microRNA-548a-5p (miR-548a-5p)/phosphatase and tensin homolog deleted on chromosome 10 (PTEN) axis mediates the cardioprotective effects of isoflurane (ISO).
Main Methods:
- An in vitro hypoxia/reoxygenation (H/R) model using H9c2 cardiomyocytes was established.
- miR-548a-5p and PTEN expression, cell viability, apoptosis, myocardial injury markers (CK-MB, cTnI, LDH), and reactive oxygen species (ROS) were assessed.
- Dual-luciferase reporter assay confirmed the direct binding between miR-548a-5p and PTEN.
Main Results:
- H/R injury downregulated miR-548a-5p and upregulated PTEN, leading to decreased cell viability, increased apoptosis, and elevated injury markers and ROS.
- Isoflurane pretreatment reversed these adverse effects by restoring miR-548a-5p and suppressing PTEN.
- Inhibition of miR-548a-5p attenuated ISO's cardioprotection, while PTEN silencing restored it, confirming the axis's role.
Conclusions:
- Isoflurane exerts cardioprotective effects against I/R injury through the miR-548a-5p/PTEN signaling pathway.
- This pathway represents a potential therapeutic target for mitigating I/R injury.
- The findings highlight the intricate molecular mechanisms involved in anesthetic-induced cardioprotection.
