ArticleNaunyn-Schmiedeberg's archives of pharmacology2020
Fibrauretine reduces ischemia/reperfusion injury via RISK/eNOS activation.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed, 3 citations in OpenAlex.
- Advances in research on the protective mechanisms of traditional Chinese medicine (TCM) in myocardial ischaemia-reperfusion injury.Pharmaceutical biology · 2022Article
- Retraction Note: Fibrauretine reduces ischemia/reperfusion injury via RISK/eNOS activation.Naunyn-Schmiedeberg's archives of pharmacology · 2021Article
Corrections and comments
- Expression of concern · 2020-05-29Concerns/Issues about Data · Updated to Retraction ·
- Retraction · 2020-12-08Concerns/Issues about Data · Investigation by Journal/Publisher · Paper Mill · Upgrade/Update of Prior Notice(s) · · see also: https://link.springer.com/article/10.1007/s00210-021-02056-8
- Retracted
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Current studies have shown that fibrauretine can be used in the treatment of cardiovascular diseases; however, the protective mechanism of fibrauretine in cardiovascular diseases is unclear. The aim of this study was to investigate the effect and mechanism of fibrauretine in acute myocardial ischemia-reperfusion injury. We investigated the effects of glucocorticoid receptor/oestrogen receptor (GR/ER)-mediated Akt phosphorylation, extracellular regulated protein kinase (ERK1/2) activation and nitric oxide (NO) on the treatment of acute myocardial ischemia-reperfusion injury by fibrauretine. Myocardial ischemia-reperfusion (I/R) injury models were established in rats and gene-knockout mice, and the infarct size was measured. We detected the expression and phosphorylation of phosphatidylinositol-3 kinase (PI3K), protein kinase B (Akt), glucocorticoid receptor, oestrogen receptor, lactate dehydrogenase (LDH), creatine phosphokinase (CK-MB), stress-activated protein kinase (JNK), P38 protein kinase (P38 MAPK) and nitric oxide synthase (NOS) with or without the inhibitors to investigate the protective effect of fibrauretine on the heart. The results showed that fibrauretine can significantly reduce the myocardial infarction area in myocardial I/R injury, inhibit the activities of LDH and CK-MB in the serum, and increase the content of NO. However, the effects of fibrauretine on the reduction of the myocardial infarction area were eliminated by the PI3K inhibitor LY294002, Akt inhibitor IV, GR inhibitor RU468, ER inhibitor tamoxifen, eNOS inhibitor L-NAME and ERK1/2 inhibitor U0126. Moreover, in the case of WT mice and gene-knockout eNOS and iNOS mice, fibrauretine was able to significantly reduce the myocardial infarction area in iNOS
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.