ArticleNaunyn-Schmiedeberg's archives of pharmacology2015
TM-1-1DP exerts protective effect against myocardial ischemia reperfusion injury via AKT-eNOS pathway.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.
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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
4 citing papers in PubMed, 1 synthesis or guideline pooled it, 7 citations in OpenAlex.
- Efficacy of Alkaloids in Alleviating Myocardial Ischemia-Reperfusion Injury in Rats: A Meta-Analysis of Animal Studies.BioMed research international · 2021Pooled it
- Mitochondrial Dysfunction in Diabetic Cardiomyopathy: The Possible Therapeutic Roles of Phenolic Acids.International journal of molecular sciences · 2020Review
- Modification of Caffeic Acid with Pyrrolidine Enhances Antioxidant Ability by Activating AKT/HO-1 Pathway in Heart.PloS one · 2016Article
- Caffeic acid ethanolamide prevents cardiac dysfunction through sirtuin dependent cardiac bioenergetics preservation.Journal of biomedical science · 2015Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Coronary heart disease remains a leading cause of death in the world. The demand on targeting therapy to reduce myocardial ischemia/reperfusion (I/R) injury is still urgent. The pathogenesis of I/R-induced myocardial injury is complicated. Reactive oxygen species (ROS) generation and inflammatory response activation participate in the development of I/R injury. Cell death occurs and finally leads to myocardial infarction. A newly phenolic aporphine alkaloid derivative, TM-1-1DP, was synthesized in our team. We aimed to investigate the effect of novel compound on myocardial I/R injury. Rats were subjected to 1-h coronary artery occlusion and followed by 2-h reperfusion. Adult rat cardimoycyte was isolated for the cell study, and H2O2 was added into culture medium to induce ROS stress. As compared to the sham group, TM-1-1DP-treated rats had better cardiac performance in association with less infarct size and cardiac injury markers after myocardial I/R. The protective effect is associated with the inhibition of inflammatory response, cell death-related pathway (caspase-3 and TNF-α), and the activation of AKT-eNOS pathway. The finding was further coincided with the cell study. TM-1-1DP treatment significantly alleviated ROS production and improved cell viability in cardiomyocyte after H2O2 exposure. The action of TM-1-1DP is via a nitric oxide (NO)-dependent manner, since NOS inhibitor, L-NAME, abolished the protective effect. We provide a new insight into this therapeutic potential for phenolic aporphine alkaloid in myocardial I/R.
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