Treatment of myocardial damage past the coronary intervention—what can be salvaged?
In the report by Li et al. in this issue of Journal of Xiangya Medicine (JXYM), 80 rats underwent either permanent ligation of the left anterior descending coronary artery or a sham operation. The animals that underwent ligation, and therefore developed an acute myocardial infarction, were subsequently treated with either placebo, low-dose salidroside or high dose salidroside. Treatment with salidroside has been previously reported to be beneficial in cerebral ischemia (1) and cancer (2). These effects are partly attributed to the anti-apoptotic properties of salidroside. Li et al. studied whether this effect could also be beneficial in the heart, following myocardial infarction after 2 weeks. Using a combination of TUNEL staining and immunoblotting and myocardial mitochondria isolation, the authors elegantly show that treatment with salidroside significantly improves survival rates and limits myocardial cell apoptosis, 2 weeks after myocardial infarction. Furthermore, Li et al. deliver evidence that this effect could be attributed to alterations in expression of genes that are known to be involved in cell apoptosis, such as Bcl-2 and cytochrome-c. Besides this they show also that salidroside limits the release of cleaved caspase-3 and -9. These two proteins play an important role in the caspase cascade, which leads to apoptosis (3). Taken together, treatment with salidroside seems to be beneficial in preserving myocardial tissue following myocardial infarction by limiting ischemia and induced cell death.