Protective Effects of Shen-Yuan-Dan, a Traditional Chinese Medicine, against Myocardial Ischemia/Reperfusion Injury In Vivo and In Vitro

Objectives. The study was to investigate the effects and mechanisms of Shen-Yuan-Dan (SYD) pharmacological postconditioning on myocardial ischemia/reperfusion (I/R) injury. Methods. In the in vivo experiment, myocardial injury markers and histopathology staining were examined. In the in vitro experi...

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Bibliographic Details
Published in:Evidence-based complementary and alternative medicine 2013-01, Vol.2013 (2013), p.1-11
Main Authors: Liu, Hong-Xu, Shang, Juju, Chu, Fuyong, Li, Aiyong, Wu, Bao, Xie, Xinran, Liu, Weihong, Yang, Hongzhi, Tong, Tong
Format: Article
Language:English
Subjects:
1-Phosphatidylinositol 3-kinase
AKT protein
Angioplasty
Animal models
Apoptosis
BAX protein
Bcl-2 protein
Cardiomyocytes
Chinese medicine
Coronary vessels
Creatine
Creatine kinase
Herbal medicine
Histopathology
Hypertension
Immunocytochemistry
Ischemia
Kinases
Laboratories
Malondialdehyde
Medical research
Myocardial ischemia
Myocardium
Reperfusion
Rodents
Staining
Superoxide dismutase
Traditional Chinese medicine
Veins & arteries
Viability
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Summary:Objectives. The study was to investigate the effects and mechanisms of Shen-Yuan-Dan (SYD) pharmacological postconditioning on myocardial ischemia/reperfusion (I/R) injury. Methods. In the in vivo experiment, myocardial injury markers and histopathology staining were examined. In the in vitro experiment, cell viability and cell apoptosis were, respectively, detected by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assays and Hoechst 33342 fluorochrome staining. The protein expressions of Bcl-2 and Bax were determined by immunocytochemistry assay. Results. Both low and high doses of SYD protected myocardium against I/R injury in rat model by reducing lactic dehydrogenase (LDH) and creatine kinase-MB (CK-MB) activity and malondialdehyde (MDA) content, increasing superoxide dismutase (SOD) activity and attenuating histopathology injury. Meanwhile, in the in vitro experiment, SYD promoted cell viability and inhibited the cardiomyocyte apoptosis. The level of Bcl-2 protein was restored to the normal level by SYD pharmacological postconditioning. In contrast, the Bax protein level was markedly reduced by SYD pharmacological postconditioning. These effects of SYD were inhibited by LY294002. Conclusions. The results of this study suggested that SYD pharmacological postconditioning has protective effects against myocardial I/R injury in both in vivo and in vitro models, which are related to activating the phosphatidylinositol 3-kinase/Akt (PI3K/Akt) pathway.
ISSN:1741-427X
1741-4288
DOI:10.1155/2013/956397