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A review of the mechanism of action of Dantonic® for the treatment of chronic stable angina.

Authors :
Liao, Wenjing
Ma, Xiaohui
Li, Ju
Li, Xinxin
Guo, Zhixin
Zhou, Shuiping
Sun, He
Source :
Biomedicine & Pharmacotherapy. Jan2019, Vol. 109, p690-700. 11p.
Publication Year :
2019

Abstract

Graphical abstract This review article mainly focuses on the mechanism of action (MoA) of Dantonic® for the treatment of chronic stable angina, which includes the promotion of coronary microcirculation, the optimization of myocardial energy metabolism and the inhibition of platelet aggregation. Highlights • Dantonic® is a currently used medicine for chronic stable angina (CSA) in China. • The mechanism of action (MoA) of Dantonic® for CSA mainly includes three aspects. • The MoA of Dantonic® for CSA includes promoting coronary microcirculation. • The MoA of Dantonic® for CSA includes optimizing myocardial energy metabolism. • The MoA of Dantonic® for CSA includes inhibiting platelet aggregation. Abstract Chronic stable angina (CSA) presents as a complication of coronary heart disease, leading to a high incidence and mortality rate worldwide. Dantonic® or Compound Danshen Dripping Pills (CDDP) is a well-known traditional Chinese medicine used for the treatment of myocardial ischemic diseases, such as angina pectoris (AP), myocardial infarction, and sudden death. Dantonic® has been extensively utilized in clinical practice in China for more than 14 years and has proved to be an effective therapy for the treatment of many myocardial ischemic diseases since its approval by CFDA in 1994. Clinical studies in China have shown that Dantonic® is an effective and safe drug for the treatment of angina pectoris manifested with ameliorating anginal symptoms and showing few adverse effects. Nevertheless, the mechanism of Dantonic® for the treatment of angina has been underestimated. Therefore, in this review, we mainly focus on discussing the pharmacological mechanism of action (MoA) of Dantonic® for the treatment of CSA, including the promotion of coronary microcirculation, the optimization of myocardial energy metabolism, and the inhibition of platelet aggregation. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
07533322
Volume :
109
Database :
Academic Search Index
Journal :
Biomedicine & Pharmacotherapy
Publication Type :
Academic Journal
Accession number :
133461802
Full Text :
https://doi.org/10.1016/j.biopha.2018.10.013