Cardioprotective effects of sinomenine in myocardial ischemia/reperfusion injury in a rat model
Saudi Pharmaceutical Journal, ISSN: 1319-0164, Vol: 30, Issue: 6, Page: 669-678
2022
- 13Citations
- 11Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
Citation Benchmarking is provided by Scopus and SciVal and is different from the metrics context provided by PlumX Metrics.
Metrics Details
- Citations13
- Citation Indexes13
- 13
- CrossRef10
- Captures11
- Readers11
- 11
Article Description
Ischemia reperfusion (I/R) play an imperative role in the expansion of cardiovascular disease. Sinomenine (SM) has been exhibited to possess antioxidant, anticancer, anti-inflammatory, antiviral and anticarcinogenic properties. The aim of the study was scrutinized the cardioprotective effect of SM against I/R injury in rat. Rat were randomly divided into normal control (NC), I/R control and I/R + SM (5, 10 and 20 mg/kg), respectively. Ventricular arrhythmias, body weight and heart weight were estimated. Antioxidant, inflammatory cytokines, inflammatory mediators and plasmin system indicator were accessed. Pre-treated SM group rats exhibited the reduction in the duration and incidence of ventricular fibrillation, ventricular ectopic beat (VEB) and ventricular tachycardia along with suppression of arrhythmia score during the ischemia (30 and 120 min). SM treated rats significantly (P < 0.001) altered the level of antioxidant parameters. SM treatment significantly (P < 0.001) repressed the level of creatine kinase MB (CK-MB), creatine kinase (CK) and troponin I (Tnl). SM treated rats significantly (P < 0.001) repressed the tissue factor (TF), thromboxane B2 (TXB2), plasminogen activator inhibitor 1 (PAI-1) and plasma fibrinogen (Fbg) and inflammatory cytokines and inflammatory mediators. Our result clearly indicated that SM plays anti-arrhythmia effect in I/R injury in the rats via alteration of oxidative stress and inflammatory reaction.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S1319016422001049; http://dx.doi.org/10.1016/j.jsps.2022.04.005; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85131247529&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/35812144; https://linkinghub.elsevier.com/retrieve/pii/S1319016422001049; https://dx.doi.org/10.1016/j.jsps.2022.04.005
Springer Science and Business Media LLC
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