ArticlePloS one2015
Influence of levosimendan postconditioning on apoptosis of rat lung cells in a model of ischemia-reperfusion injury.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 29 citations in OpenAlex.
- The effect of post-reperfusion levosimendan in an experimental intestinal ischemia-reperfusion model.Journal of anesthesia, analgesia and critical care · 2022Article
- Lung injury after cardiopulmonary bypass: Alternative treatment prospects.World journal of clinical cases · 2022Review
- Levosimendan-induced venodilation is mediated by opening of potassium channels.ESC heart failure · 2021Review
- Ex Vivo Lung Perfusion with K(ATP) Channel Modulators Antagonize Ischemia Reperfusion Injury.Cells · 2021Article
- Intranasal levosimendan prevents cognitive dysfunction and apoptotic response induced by repeated isoflurane exposure in newborn rats.Naunyn-Schmiedeberg's archives of pharmacology · 2021Article
- Bag-1L Protects against Cell Apoptosis in an In Vitro Model of Lung Ischemia-Reperfusion Injury through the C-Terminal "Bag" Domain.BioMed research international · 2021Article
- Isosamidin fromAntioxidants (Basel, Switzerland) · 2020Article
- Anti-apoptosis effect of heme oxygenase-1 on lung injury after cardiopulmonary bypass.Journal of thoracic disease · 2020Article
- Levosimendan Protects against Doxorubicin-Induced Cardiotoxicity by Regulating the PTEN/Akt Pathway.BioMed research international · 2020Article
- Lung injury after asphyxia and hemorrhagic shock in newborn piglets: Analysis of structural and inflammatory changes.PloS one · 2019Article
- TT-1, an analog of melittin, triggers apoptosis in human thyroid cancer TT cells via regulating caspase, Bcl-2 and Bax.Oncology letters · 2018Article
- Ubiquinol-cytochrome c reductase core protein 1 may be involved in delayed cardioprotection from preconditioning induced by diazoxide.PloS one · 2017Article
- Resolvin D1 Alleviates the Lung Ischemia Reperfusion Injury via Complement, Immunoglobulin, TLR4, and Inflammatory Factors in Rats.Inflammation · 2016Article
- Assessment of expressions of Bcl-XL, b-FGF, Bmp-2, Caspase-3, PDGFR-α, Smad1 and TGF-β1 genes in a rat model of lung ischemia/reperfusion.Iranian journal of basic medical sciences · 2016Article
- [Dexmedetomidine preconditioning protects against lung injury in hemorrhagic shock rats].Brazilian journal of anesthesiology (Elsevier)Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveTo ascertain if levosimendan postconditioning can alleviate lung ischemia-reperfusion injury (LIRI) in rats.
methodOne hundred rats were divided into five groups: Sham (sham), ischemia-reperfusion group (I/R group), ischemic postconditioning (IPO group), levosimendan postconditioning (Levo group) and combination postconditioning group of levosimendan and 5-Hydroxydecanoic acid (Levo+5-HD group). The apoptotic index (AI) of lung tissue cells was determined using the terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay. Expression of active cysteine aspartate specific protease-3 ( active caspase-3), Bcl-2 and Bax in lung tissue was determined by immunohistochemical staining. The morphopathology of lung tissue was observed using light and electron microscopy.
resultsAI values and expression of active caspase-3, Bcl-2 and Bax of lung tissue in I/R and Levo+5-HD groups were significantly higher than those in the sham group ( P<0.05). AI values and expression of active caspase-3 and Bax were significantly lower, whereas that of Bcl-2 was higher significantly in the Levo group, compared with I/R and Levo+5-HD groups (P<0.05). Significant differences were not observed in comparisons between I/R and Levo+5-HD groups as well as IPO and Levo groups.
conclusionLIRI can be alleviated by levosimendan, which simulates an IPO protective function. A postulated lung-protective mechanism of action could involve opening of mitochondrial adenosine triphosphate-sensitive potassium channels, relieving Ca2+ overload, upregulation of expression of Bcl-2, and downregulation of expression of active caspase-3 and Bax.
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