Protective Effects of Shen-Yuan-Dan, a Traditional Chinese Medicine, against Myocardial Ischemia/Reperfusion InjuryIn VivoandIn Vitro | Zendy

Hongxu Liu | Zendy; Juju Shang | Zendy; Fuyong Chu | Zendy; Aiyong Li | Zendy; Bao Qiang Wu | Zendy; Xinran Xie | Zendy; Weihong Liu | Zendy; Hongzhi Yang | Zendy; Tong Tong | Zendy

Open Access

Protective Effects of Shen-Yuan-Dan, a Traditional Chinese Medicine, against Myocardial Ischemia/Reperfusion InjuryIn VivoandIn Vitro

Author(s) -

Hongxu Liu,

Juju Shang,

Fuyong Chu,

Aiyong Li,

Bao Qiang Wu,

Xinran Xie,

Weihong Liu,

Hongzhi Yang,

Tong Tong

Publication year - 2013

Publication title -

evidence-based complementary and alternative medicine

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 0.552

H-Index - 90

eISSN - 1741-4288

pISSN - 1741-427X

DOI - 10.1155/2013/956397

Subject(s) - in vivo , viability assay , lactate dehydrogenase , reperfusion injury , pharmacology , apoptosis , creatine kinase , superoxide dismutase , protein kinase b , pi3k/akt/mtor pathway , medicine , in vitro , chemistry , ischemia , biochemistry , biology , oxidative stress , enzyme , microbiology and biotechnology

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.

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