ArticleMolecular biology reports2009
Protective effects of N-acetylcysteine in isoproterenol-induced myocardium injury in rats.
Article in Molecular biology reports, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
6 citing papers in PubMed, 16 citations in OpenAlex.
- Role of M6a Methylation in Myocardial Ischemia-Reperfusion Injury and Doxorubicin-Induced Cardiotoxicity.Cardiovascular toxicology · 2024Review
- N-acetylcysteine alleviates post-resuscitation myocardial dysfunction and improves survival outcomes via partly inhibiting NLRP3 inflammasome induced-pyroptosis.Journal of inflammation (London, England) · 2020Article
- N-acetylcysteine tiherapeutically protects against pulmonary fibrosis in a mouse model of silicosis.Bioscience reports · 2019Article
- N-acetylcysteine (NAC) ameliorates Epstein-Barr virus latent membrane protein 1 induced chronic inflammation.PloS one · 2017Article
- Protective effect of Spirulina against 4-nitroquinoline-1-oxide induced toxicity.Molecular biology reports · 2011Article
- Effect of genetic variants of chemokine receptors on the development of myocardial infarction in Turkish population.Molecular biology reports · 2010Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Isoproterenol (ISO) has been found to cause severe injury in the myocardium. The aim of this study was to investigate the protective effects of N-acetylcysteine (NAC) on ISO-induced myocardial injury in rats and its underlying mechanisms. Fouty male Wistar rats were randomly divided into four groups: control, ISO, NAC, and ISO + NAC group. Myocardial histopathological observation were performed; The activities of creatine kinase isoenzyme-MB (CK-MB) and lactate dehydrogenase (LDH) were examined; Myocardium TNF-alphaand IL-1beta gene expressions were examined by RT-PCR analysis; Myocardial expressions of TNF-alphaand IL-1betaproteins were observed by immunohistochemical assay and western blotting analysis. The myocardial injury induced by ISO was significantly reduced by the treatment of NAC as judged by the reduction of myocardial necrosis. Compared with ISO group, rats pre-injected with NAC showed a significant decrease in the activities of cardiac marker enzymes such as CK-MB and LDH in serum. NAC inhibits the pro-inflammatory factors expressions (TNF-alphaand IL-1beta) stimulated by ISO. In conclusion, NAC exerts significant cardio-protective effects against ISO-induced myocardial injury in rats, likely regulating pro-inflammatory factors expressions.
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Registered trials
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