Objective To investigate the role and mechanisms of platelet microparticles ( PMP) sin vascular endothelial injury of the diabetic aorta. Methods SD rats were randomly divided into the normal (NC) and diabetic (DM) groups. PMPs were isolated and purified. Next, primary cultured endothelial cells were transfected with microRNA (miR)-4306 to detect PMPs in vascular endothelial cells. The effects of activity and the effects on the miR-4306 / vascular endothelial growth factor A ( VEGFA) / extracellular signal-regulated kinase ( ERK) 1 / 2 / nuclear factor κB ( NF-κB) signaling pathway were evaluated. Results The positive expression and apoptosis rates of endothelial nitric oxide synthase (eNOS) and caspase-3 in the DM group were significantly different from those in the NC group (P<0. 05 or P<0. 01). The relative expression of miR-4306 in the mimic-M group and inhibitor-M group was significantly different from that in the miR-M group (t= 3. 821, 4. 597, P<0. 05 or P<0. 01). Moreover, the relative expression of miR-4306 in the mimic-M group was significantly different from that in the inhibitor-M group (P<0. 01). The relative expression of miR-4306 in M group was significantly different from that in Ctrl group (P<0. 01). In addition, the relative expression of VEGFA, NF- κBp65, p-IκBα and p-ERK in the mimic-M group and inhibitor-M group was significantly different from that in M group(P<0. 05 or P<0. 01). The relative expression of VEGFA, NF-κBp65, p-IκBα and p-ERK in the M group was significantly different from that of Crtl group (P<0. 05 or P<0. 01). Conclusions PMPs may cause endothelial damage in the diabetic aorta, the underlying mechanism may be related to the activation of miR-4306 / VEGFA/ ERK1 / 2 / NF-κB signaling.