Amelioration of acute myocardial infarction by the saponins from flower of Panax notoginseng via promoting of angiogenesis and protecting apoptosis

Ischemic heart disease can lead to an irreversible myocardium death and no effective treatment is available for structural and functional recovery. Angiogenesis therapy could be effective to ameliorate post-ischemic conditions by restoring blood supply to damaged tissues so as to alleviate or restore the dysfunctions. The root of Panax notoginseng is traditionally used as an anti-haemorrhagic agent to promote blood circulation without causing “congealed” blood [1,2]. On the contrary, the flower of P. notoginseng is folk used on the prevention of hypertension and normalizing abnormal blood cholesterol profile but the pharmacological studies on the flower of P. notoginseng is limited [3] Interestingly, the flower of P. notoginseng contains higher abundance of saponins particularly protopanaxadiol-type ginsenosides than root [4]. Therefore, in this study, anti-myocardial infarction effect of total saponins from the flower of P. notoginseng (FS) was determined. Our results demonstrated that the post-treatment of rat myocardial infarction (MI) model with FS (25 – 50 mg/kg/day) for two weeks could activate the mRNA expression of VEGF by approximately 3 folds and enhance the blood vessel density formation in peri-infarct area of the heart by 50.7% and 41.4% versus MI group, respectively. Moreover, TUNEL staining showed that the average number of apoptotic nuclei per field in peri-infarct myocardium for FS 25 and FS 50 groups were 13.6 and 12.3 compared to 14.9 for MI group. In addition, FS significantly promoted VEGF induced the migration of human umbilical vein endothelial cells (HUVEC) as well as restored the defective intersegmental vessels (ISV) in chemically induced blood vessel damage model in zebrafish larva. Taken together, FS promoted angiogenesis in a blood vessel damage model in zebrafish and a myocardial infarction model in rat and hence has the potential to be developed as a new anti-Cardiovascular diseases (CVD) agent.