Protective Effect of Sufentanil on Myocardial Ischemia-Reperfusion Injury in Rats by Inhibiting Endoplasmic Reticulum Stress

Abstract

Objective. Sufentanil is the most common drug in clinical practice for the treatment of ischemic heart disease. This study is to investigate the protective mechanism of sufentanil on rat myocardial ischemia-reperfusion (I/R) injury. Methods. A rat I/R model was established by ligating the left anterior descending coronary artery. A total of 24 SD male rats were enrolled and divided randomly into the control group, I/R group, sufentanil group (SUF; 3 μg/kg), and diltiazem group (DLZ; 20 mg/kg; positive control). The rat hearts were subjected to 30 min of ischemia followed by 120 min of reperfusion. Subsequently, hemodynamics, pathological changes of myocardial tissue, serum biochemical parameters, oxidative stress factors, the level of serum inducible nitric oxide synthases (iNOS), interleukin-6 (IL-6), and other bioactive factors were analyzed in the rats. Result. Compared with the I/R group, sufentanil significantly improved cardiac action, myocardial fiber, and cardiomyocyte morphology and reduced inflammatory cell infiltration in rats in the SUF group. And the level of creatine kinase isoenzyme (CK-MB), troponin (cTn), lactate dehydrogenase (LDH), malondialdehyde (MDA), iNOS, and IL-6 was significantly declined in the serum of SUF group, while the activities of glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) were significantly activated in the myocardial tissues. In addition, sufentanil also significantly decreased the protein expression of GRP78, CHOP, Caspase 12, and ATF6 in the myocardial tissue of the SUF group. Conclusion. Sufentanil has a significant protective activity on myocardial I/R injury in rats, the mechanism of which may be associated with the inhibition of endoplasmic reticulum stress and oxidative stress.

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

“…Wu et al reported that sufentanil pretreatment could prevent myocardial I/R injury via the miR-125a/DRAM2 axis [ 37 ]. In I/R rats, sufentanil alleviates myocardial injury and plays a protective role by inhibiting oxidative stress, inflammatory response, and endoplasmic reticulum stress [ 14 ]. Therefore, further exploration to sufentanil is required.…”

“…Studies reveal that sufentanil plays an important protective role in myocardial I/R injury [ 10 – 12 ]. Sufentanil has obvious protective effect on myocardial I/R injury in rats, and its mechanism may be related to activation of the ERK1/2 pathway and the inhibition of endoplasmic reticulum stress and oxidative stress [ 13 , 14 ]. In addition, a study by Li et al indicated a protective effect of sufentanil on skeletal muscle atrophy in septic patients [ 15 ].…”

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

“…Increases in the levels of stress hormones, such as NE and E, indicate increased sympathetic nerve activity, and their entry into the bloodstream may cause vasoconstriction and trigger hemodynamic instability[ 26 ]. Ang Ⅱ activates the renin–angiotensin system and induces oxidative stress[ 27 ]. SOD exerts antioxidant effects by scavenging oxygen free radicals to reduce oxidative stress[ 28 ].…”

Retracted: Protective Effect of Sufentanil on Myocardial Ischemia‐Reperfusion Injury in Rats by Inhibiting Endoplasmic Reticulum Stress

“…This article has been retracted by Hindawi following an investigation undertaken by the publisher [1]. This investigation has uncovered evidence of one or more of the following indicators of systematic manipulation of the publication process:…”

“…This article has been retracted by Hindawi following an investigation undertaken by the publisher [ 1 ]. This investigation has uncovered evidence of one or more of the following indicators of systematic manipulation of the publication process: Discrepancies in scope Discrepancies in the description of the research reported Discrepancies between the availability of data and the research described Inappropriate citations Incoherent, meaningless and/or irrelevant content included in the article Peer-review manipulation …”