Panax notoginseng saponin is superior to aspirin in inhibiting platelet adhesion to injured endothelial cells through COX pathway in vitro

Objective This study was designed to investigate the effect of Panax notoginseng saponin (PNS) on platelet adhesion to injured endothelial cells (ECs) and platelet activation induced by injured ECs, and to explore its underlying mechanisms. Methods Human umbilical vein endothelial cells (HUVECs) pretreated with aspirin (ASA,15 μg/mL) or PNS (160 μg/mL), or neither, were exposed to oxidized low-density lipoprotein (ox-LDL,80 mg/L) for 16 h. Platelets were then added and co-cultured with HUVECs for 5 min. Platelet adhesion to ECs, platelet CD62p expression, and HUVEC apoptosis were assessed by fluorescence activated cell sorting (FACS)·Supernatant concentration of 6-keto-PGF1α and thromboxane 2 (TXB2) were measured by radioimmunoassay. Cyclooxygenase-1 (COX-1) and COX-2 protein expression were measured by western blotting. Results The inhibitory effect of PNS on platelet activation was similar to ASA, but the inhibitory effect of PNS on platelet adhesion to ECs was superior to ASA. PNS modulated COX-2 expression, and increased 6-keto-PGF1α concentration in HUVECs, while down-regulated COX-1 expression and decreased supernatant TXB2 concentration in platelets. Co-culturing of injured HUVECs with platelets increased HUVEC apoptosis induced by ox-LDL compared with HUVECs cultured without platelets; ASA increased HUVEC apoptosis induced by ox-LDL when cultured without platelets, while decreased the apoptosis when co-cultured with platelets. Conclusions EC protection by ASA is closely associated with its inhibitory effect on platelet activation. PNS is superior to ASA in protecting ECs and in inhibiting platelet adhesion to injured ECs, and the regulation of COX pathway in both ECs and platelets might be the underlying mechanisms of PNS.