» Articles » PMID: 35774755

Sufentanil Alleviates Sepsis-Induced Myocardial Injury and Stress Response in Rats Through the ERK/GSK-3 Signaling Axis

Overview
Authors
Affiliations
Soon will be listed here.
Abstract

Objective: To explore the effect and possible mechanism of sufentanil on sepsis-induced myocardial injury and stress response in rats.

Methods: The cecal ligation and puncture (CLP) method was utilized to establish the sepsis model of rats to explore the effect of sufentanil pretreatment with different concentrations on myocardial injury and oxidative stress in CLP rats. Echocardiogram was applied for detecting cardiac hemodynamic parameters in rats; hematoxylin and eosin (HE) staining as well as TUNEL staining was done for observing pathological changes of myocardial tissue and cardiomyocyte apoptosis in rats, respectively; biochemical testing and enzyme-linked immunosorbent assay (ELISA) were done for determining myocardial injury marker level in serum, oxidative stress substances in myocardial tissue, and neuroendocrine hormone level in serum of rats, respectively; finally, Western blot was performed for checking the expression level of ERK/GSK-3 signaling pathway-related proteins in myocardial tissue of rats.

Results: A model of rat with sepsis-induced myocardial injury was constructed with the CLP method. Specifically, this rat model was characterized by obvious cardiac function and tissue damage, cardiomyocyte apoptosis, and oxidative stress response. Sufentanil pretreatment significantly improved cardiac function injury, alleviated pathological injury and oxidative stress response in myocardial tissue, and inhibited cardiomyocyte apoptosis. Specifically, after sufentanil pretreatment, left ventricular end-diastolic dimension (LVEDD) and left ventricular end-systolic dimension (LVESD) were downregulated, and left ventricular ejection fraction (LVEF) was upregulated; the level of -type natriuretic peptide (BNP) of serum, creatine kinase isoenzyme (CK-MB), and troponin (cTnl) decreased; besides, malondialdehyde (MDA) level was declined, while activities of superoxide dismutase (SOD) and catalase (CAT) were increased. What is more, further mechanism exploration also revealed that sufentanil could reverse the activity of the sepsis-induced ERK/GSK-3 signaling pathway.

Conclusion: Sufentanil has an obvious protective effect on myocardial injury and stress response in CLP rats, and this protective effect may be related to the activation of the ERK/GSK-3 signaling pathway.

Citing Articles

Protective effect and mechanism of Sufentanil on acute lung injury in septic mice.

Hou H, Jiang B, Zhu A, Hou J, Qu Z, Liu R Front Pharmacol. 2025; 15:1514602.

PMID: 39885929 PMC: 11780379. DOI: 10.3389/fphar.2024.1514602.


Case report: Anesthesia management for surgical treatment of glucagonoma with symptom of characterized necrolytic migratory erythema.

Xia D, Shen L Front Oncol. 2025; 14:1408506.

PMID: 39749032 PMC: 11693641. DOI: 10.3389/fonc.2024.1408506.


Impact of thoracic paravertebral block and sufentanil on outcomes and postoperative cognitive dysfunction in thoracoscopic lung cancer surgery.

Wang D, Wang H, Zhu Y, Lu X World J Psychiatry. 2024; 14(6):894-903.

PMID: 38984344 PMC: 11230086. DOI: 10.5498/wjp.v14.i6.894.


Retracted: Sufentanil Alleviates Sepsis-Induced Myocardial Injury and Stress Response in Rats through the ERK/GSK-3 Signaling Axis.

And Alternative Medicine E Evid Based Complement Alternat Med. 2023; 2023:9854369.

PMID: 37565231 PMC: 10412208. DOI: 10.1155/2023/9854369.

References
1.
Hu Q, Wang Q, Han C, Yang Y . Sufentanil attenuates inflammation and oxidative stress in sepsis-induced acute lung injury by downregulating KNG1 expression. Mol Med Rep. 2020; 22(5):4298-4306. PMC: 7533471. DOI: 10.3892/mmr.2020.11526. View

2.
Han T, Zhou S, Li J, Tian F, Mu Y, Jing J . Homocysteine is associated with the progression of non-culprit coronary lesions in elderly acute coronary syndrome patients after percutaneous coronary intervention. J Geriatr Cardiol. 2016; 13(4):299-305. PMC: 4921541. DOI: 10.11909/j.issn.1671-5411.2016.04.010. View

3.
Angelova P, Abramov A . Role of mitochondrial ROS in the brain: from physiology to neurodegeneration. FEBS Lett. 2018; 592(5):692-702. DOI: 10.1002/1873-3468.12964. View

4.
Gotts J, Matthay M . Sepsis: pathophysiology and clinical management. BMJ. 2016; 353:i1585. DOI: 10.1136/bmj.i1585. View

5.
Zeng X, Liu D, Han Y, Huang Z, Zhang J, Huang Q . Assessment of inflammatory markers and mitochondrial factors in a rat model of sepsis-induced myocardial dysfunction. Am J Transl Res. 2020; 12(3):901-911. PMC: 7137057. View