In vitro activity: Danshensu reduces lipid peroxidation on mitochondrial membrane by scavenging free radicals, and inhibits permeability and transmission of mitochondrial membrane by reducing thiol oxidation. Danshensu markedly improves cell viability and decreased lactate dehydrogenase (LDH) release in H9c2 cardiomyocytes. Danshensu increases phosphorylation of Akt and extracellular signal-related kinase 1/2 (ERK1/2) in H9c2 cells, and the protective effects of Danshensu are partially inhibited by phosphatidylinositol 3'-kinase (PI3K) specific inhibitor wortmannin or ERK specific inhibitor U0126. Danshensu could provide significant cardioprotection against MI/R injury, and the potential mechanisms might to suppression of cardiomyocytes apoptosis through activating the PI3K/Akt and ERK1/2 signaling pathways. Danshensu increases Bcl-2 expression and decreases Bax, active caspase-3 expression by activating Akt and ERK signaling pathways. Danshensu has been demonstrated to have biological activities in improving microcirculation, suppressing the formation of reactive oxygen species, inhibiting platelet adhesion and aggregation, protecting myocardium against ischemia, protecting endothelial cells against injury induced by inflammation.

Cell Assay: Cardiomyocytes are exposed to ischemia by replacing medium with an 'ischemic buffer', this buffer is designed to simulate the extracellular milieu of myocardial ischemia, with the approximate concentrations of potassium, hydrogen, and lactate ions occurring in vivo. Cells are incubated in the hypoxic/ischemic chamber at 37℃ for 2 h in a humidified atmosphere of 5% CO2 and 95% nitrogen. At the onset of reperfusion, cardiomyocytes are randomly exposed to one of the following treatments: vehicle, Danshensu (1 μM or 10 μM), Danshensu plus the PI3K inhibitor wortmannin (10 nM), Danshensu plus the ERK inhibitor U0126 (10 μM). Simultaneously, in the control group, H9c2 cardiomyocytes are cultured under normal conditions in CO2 incubation.