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Inhibition of Collagen-Induced Platelet Aggregation by the Secobutanolide Secolincomolide A from Lindera obtusiloba Blume

Overview of attention for article published in Frontiers in Pharmacology, August 2017
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Title
Inhibition of Collagen-Induced Platelet Aggregation by the Secobutanolide Secolincomolide A from Lindera obtusiloba Blume
Published in
Frontiers in Pharmacology, August 2017
DOI 10.3389/fphar.2017.00560
Pubmed ID
Authors

Sang-Hyuk Jung, Joo-Hui Han, Hyun-Soo Park, Jung-Jin Lee, Seo Young Yang, Young Ho Kim, Kyung-Sun Heo, Chang-Seon Myung

Abstract

Atherothrombosis is one of the main underlying cause of cardiovascular diseases. In addition to treating atherothrombosis with antithrombotic agents, there is growing interest in the role of natural food products and biologically active ingredients for the prevention and treatment of cardiovascular diseases. This study aimed to investigate the effect of secolincomolide A (3) isolated from Lindera obtusiloba Blume on platelet activity and identify possible signaling pathways. In our study, the antiplatelet activities of 3 were measured by collagen-induced platelet aggregation and serotonin secretion in freshly isolated rabbit platelets. Interestingly, 3 effectively inhibited the collagen-induced platelet aggregation and serotonin secretion via decreased production of diacylglycerol, arachidonic acid, and cyclooxygenase-mediated metabolites such as thromboxane B2 (TXB2), and prostaglandin D2 (PGD2). In accordance with the antiplatelet activities, 3 prolonged bleeding time and attenuated FeCl3-induced thrombus formation in arterial thrombosis model. Notably, 3 abolished the phosphorylation of phospholipase Cγ2 (PLCγ2), spleen tyrosine kinase (Syk), p47, extracellular signal-regulated kinase 1/2 (ERK1/2), protein kinase B (Akt) by inhibiting the activation of the collagen receptor, glycoprotein VI (GPVI). Taken together, our results indicate the therapeutic potential of 3 in antiplatelet action through inhibition of the GPVI-mediated signaling pathway and the COX-1-mediated AA metabolic pathways.

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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 21 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 21 100%

Demographic breakdown

Readers by professional status Count As %
Student > Bachelor 5 24%
Student > Ph. D. Student 3 14%
Other 2 10%
Researcher 2 10%
Student > Doctoral Student 1 5%
Other 2 10%
Unknown 6 29%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 3 14%
Pharmacology, Toxicology and Pharmaceutical Science 3 14%
Chemistry 2 10%
Medicine and Dentistry 2 10%
Agricultural and Biological Sciences 2 10%
Other 3 14%
Unknown 6 29%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 23 August 2017.
All research outputs
#20,444,703
of 22,999,744 outputs
Outputs from Frontiers in Pharmacology
#10,193
of 16,305 outputs
Outputs of similar age
#277,223
of 317,366 outputs
Outputs of similar age from Frontiers in Pharmacology
#157
of 250 outputs
Altmetric has tracked 22,999,744 research outputs across all sources so far. This one is in the 1st percentile – i.e., 1% of other outputs scored the same or lower than it.
So far Altmetric has tracked 16,305 research outputs from this source. They receive a mean Attention Score of 5.0. This one is in the 1st percentile – i.e., 1% of its peers scored the same or lower than it.
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We're also able to compare this research output to 250 others from the same source and published within six weeks on either side of this one. This one is in the 1st percentile – i.e., 1% of its contemporaries scored the same or lower than it.