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Salvianolic Acid A Ameliorates Arsenic Trioxide-Induced Cardiotoxicity Through Decreasing Cardiac Mitochondrial Injury and Promotes Its Anticancer Activity

Overview of attention for article published in Frontiers in Pharmacology, May 2018
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Title
Salvianolic Acid A Ameliorates Arsenic Trioxide-Induced Cardiotoxicity Through Decreasing Cardiac Mitochondrial Injury and Promotes Its Anticancer Activity
Published in
Frontiers in Pharmacology, May 2018
DOI 10.3389/fphar.2018.00487
Pubmed ID
Authors

Jing-yi Zhang, Min Wang, Rui-ying Wang, Xiao Sun, Yu-yang Du, Jing-xue Ye, Gui-bo Sun, Xiao-bo Sun

Abstract

Arsenic trioxide (ATO) is used as a therapeutic agent in the treatment of acute promyelocytic leukemia (APL). The therapeutic use of arsenic is limited due to its severe cardiovascular side effects. The cardio-protective effect of salvianolic acid A (Sal A) against ATO cardiotoxicity has been reported. However, the distinct role of the mitochondria in the cardio-protection of Sal A is not understood. The aim of this study was to determine whether Sal A preconditioning protects against ATO-induced heart injury by maintaining cardiac mitochondrial function and biogenesis. For the in vivo study, BALB/c mice were treated with ATO and/or Sal A. For the in vitro study, we determined the effects of ATO and/or Sal A in H9c2 cardiomyocytes. Our results showed that ATO induced mitochondrial structural damage, abnormal mitochondrial permeability transition pore (mPTP) opening, overproduction of mitochondrial reactive oxygen species (ROS), and decreased the ATP content. Sal A pretreatment alleviated the ATO-induced mitochondrial structural and functional damage. In this study, ATO decreased the expression level of the peroxisome proliferator activator receptor gamma-coactivator 1 (PGC-1α) and disrupted the normal division and fusion of mitochondria. Sal A pretreatment improved the dynamic balance of the damaged mitochondrial biogenesis. Moreover, the combination treatment of Sal A and ATO significantly enhanced the ATO-induced cytotoxicity of SGC7901, HepaRG, K562 and HL60 cells in vitro. These results indicated that Sal A protects the heart from ATO-induced injury, which correlates with the modulation of mitochondrial function, and the maintenance of normal mitochondrial biogenesis.

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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 17 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 17 100%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 5 29%
Researcher 3 18%
Professor 2 12%
Student > Master 1 6%
Student > Postgraduate 1 6%
Other 0 0%
Unknown 5 29%
Readers by discipline Count As %
Pharmacology, Toxicology and Pharmaceutical Science 4 24%
Medicine and Dentistry 4 24%
Biochemistry, Genetics and Molecular Biology 3 18%
Unknown 6 35%
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 17 May 2018.
All research outputs
#20,492,220
of 23,055,429 outputs
Outputs from Frontiers in Pharmacology
#10,282
of 16,383 outputs
Outputs of similar age
#288,125
of 327,415 outputs
Outputs of similar age from Frontiers in Pharmacology
#235
of 409 outputs
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So far Altmetric has tracked 16,383 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 409 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.