Platelet-rich plasma (PRP) contains a variety of cytokines, some of which ameliorate oX-LDL (oxidized low-density lipoprotein)-induced endothelial cell (EC) injury. Therefore, we hypothesized that PRP might alleviate oX-LDL-induced injury.
Methodology: Human umbilical vein endothelial cells (HUVECs) were divided into four groups: a PPP (platelet-poor plasma) group, an oX-LDL group, an oX-LDL+PRP group and a PRP group. CCK-8 (Cell Counting Kit) assay, Annexin V-FITC/7-AAD and Hochest 33342 staining were performed to assess cell proliferation and apoptosis. Tube formation and cell migration assays were performed to evaluate HUVEC-mediated vasculogenesis and migration. Expression levels of Bcl-2, Bax, caspase-3, cleaved caspase-3, PI3K, Akt, eNOS p-Akt, p-eNOS, IL-6 and IL-1 were detected by western blotting or immunofluorescence.
Principal findings: PRP promoted HUVEC proliferation in a non-linear pattern, protected HUVECs against oX-LDL-induced apoptosis and attenuated oX-LDL-mediated inhibition of HUVEC migration and vasculogenesis. Additionally, compared to the PPP group, PRP downregulated pro-apoptotic proteins (ratio of Bax/Bcl-2, caspase-3 and cleaved caspase-3) as well as IL-6 and IL-1. Moreover, the PI3K/Akt/eNOS pathway was activated by PRP and inactivated by oX-LDL.
Conclusions: It was demonstrated that PRP protected HUVECs against oX-LDL-induced injury and that the PI3K/Akt/eNOS pathway was activated in this process.
Keywords: HUVECs; PI3K/Akt/eNOS; Platelet-rich plasma; oX-LDL.