Salvianolic Acid A Demonstrates Cardioprotective Effects in Rat Hearts and Cardiomyocytes After Ischemia/Reperfusion Injury

• DOI: 10.1097/fjc.0b013e31822de355
• Publication Date: 2011-07-27T09:04:31Z
• Authors: Huanjun Pan; Dongye Li; Fang Fang; Dan Chen; Lingling Qi; Ruiqu Zhang; Tongda Xu; Hong Sun
• Keywords: Male; 0301 basic medicine; Cardiotonic Agents; L-Lactate Dehydrogenase; Caspase 3; Cell Survival; Myocardium; Myocardial Infarction; Apoptosis; Heart; In Vitro Techniques; Myocardial Contraction; Perfusion; Necrosis; 03 medical and health sciences; Caffeic Acids; Heart Rate; Lactates; Animals; Myocytes, Cardiac; Phosphorylation; Cell Shape

Salvianolic acid A (Sal A), the water-soluble component from the root of the Salvia miltiorrhiza plant, possesses antioxidant, antiproliferative, and antiplatelet properties. However, whether it plays a role in the protection against ischemia-reperfusion (I/R) injury in rat hearts has yet to be elucidated. In the present study, we tested cell viability, shortening amplitude, necrosis, apoptosis, and the expression levels of Akt, phosphorylated Akt, Bcl-2, Bax, and caspase-3 after 3-hour simulated ischemia and 2- or 6-hour simulated reperfusion in cardiomyocytes. We further observed the contractile function and infarct size in isolated hearts after they were subjected to global 30-minute ischemia and 120-minute reperfusion. Pretreatment with Sal A markedly increased cell viability and shortening amplitude while reducing evidence of necrosis and apoptosis in the cells. In addition, the expression of Bcl-2 was upregulated and Bax was downregulated, thereby increasing the Bcl-2/Bax ratio. Sal A inhibited the activation of caspase-3 as well. The results also showed that Sal A significantly increased phosphorylation of Akt and that this phosphorylation can be partially inhibited by phosphoinositide 3-kinase/Akt inhibitor. Furthermore, Sal A improved I/R-induced myocardial contractile function and reduced infarct size. In summary, our results showed that Sal A prevents I/R-induced myocardial damage by reducing necrosis and apoptosis in isolated rat hearts and cardiomyocytes.