We investigated the effects of edaravone, a free radical scavenger, on peripheral nerve ischemia-reperfusion injury caused by ligation of vessels supplying the sciatic and tibial nerves in rats. The control group was administered a placebo, the standard-dose group was given 3 mg/kg of edaravone intraperitoneally every 24 hours, and the low-dose group was given 1 mg/kg of edaravone. At 7 days after reperfusion, neurological and electrophysiological parameters were improved in the standard-dose group as compared with the control group. After 14 days, however, these differences were no longer observed. After 21 days, persistent edema and nerve fiber degeneration were noted in the standard-dose group, but not in the control or low-dose groups. Edaravone was effective during the early reperfusion period, but chronic inhibition of reactive oxygen species may be detrimental for nerve regeneration after ischemia-reperfusion injury. Further studies are necessary to confirm the long-term influence of edaravone.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1002/mus.21388 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Cardiac-targeted delivery of a novel Drp1 inhibitor for acute cardioprotection.
J Mol Cell Cardiol Plus
September 2024
O'Brien Institute Department, St Vincent's Institute of Medical Research, Victoria 3065, Australia.
Dynamin-related protein 1 (Drp1) is a mitochondrial fission protein and a viable target for cardioprotection against myocardial ischaemia-reperfusion injury. Here, we reported a novel Drp1 inhibitor (DRP1i1), delivered using a cardiac-targeted nanoparticle drug delivery system, as a more effective approach for achieving acute cardioprotection. DRP1i1 was encapsulated in cubosome nanoparticles with conjugated cardiac-homing peptides (NanoDRP1i1) and the encapsulation efficiency was 99.
View Article and Find Full Text PDFMyocardial overexpression of protein phosphatase 2A-B56α improves resistance against ischemia-reperfusion injury.
J Mol Cell Cardiol Plus
March 2023
Institut für Pharmakologie und Toxikologie, Westfälische Wilhelms-Universität Münster, Domagkstr. 12, 48149 Münster, Germany.
Protein phosphatase 2A (PP2A) plays a central role in myocardial ischemia-reperfusion (I/R) injury. Several studies showed a detrimental function of PP2A by using either overexpression models of the catalytic subunit (PP2Ac) or exogenous inhibitors of PP2Ac. However, all of these approaches underestimate the contribution of regulatory B subunits in modulating the PP2A holoenzyme.
View Article and Find Full Text PDFIntegrated Analysis and Validation of Ferroptosis-Related Genes Associated with Ischemia/Reperfusion Injury in Lung Transplantation.
J Inflamm Res
January 2025
Department of Respiratory and Critical Care Medicine, Renmin Hospital of Wuhan University, Wuhan, Hubei, 430060, People's Republic of China.
Background: Lung transplantation is the only effective therapeutic option for patients with end-stage lung disease. However, ischemia/reperfusion injury (IRI) during transplantation is a leading cause of primary graft dysfunction (PGD). Ferroptosis, a form of iron-dependent cell death driven by lipid peroxidation, has been implicated in IRI across various organs.
View Article and Find Full Text PDFSpontaneous coronary artery dissection (SCAD) is characterized by intramural hematoma in a coronary artery leading to partial or complete vessel obstruction. A 51-year-old female was hospitalized with acute myocardial infarction and cardiogenic shock. She was diagnosed with severe SCAD, affecting the proximal left coronary artery.
View Article and Find Full Text PDFCirculating autophagy regulator Rubicon is linked to increased myocardial infarction risk.
J Mol Cell Cardiol Plus
March 2025
Center for Clinical Investigation (CIC1436)/CARDIOMET, Rangueil University Hospital, Toulouse, France.
Background: The identification of new biomarkers that improve existing cardiovascular risk prediction models for acute coronary syndrome is essential for accurately identifying high-risk patients and refining treatment strategies. Autophagy, a vital cellular degradation mechanism, is important for maintaining cardiac health. Dysregulation of autophagy has been described in cardiovascular conditions such as myocardial ischemia-reperfusion injury, a key factor in myocardial infarction (MI).
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!