Effects of reduced β2 glycoprotein I on high glucose‑induced cell death in HUVECs.

Reduced β2 glycoprotein I (β2GPI) has been demonstrated to exhibit a beneficial effect in diabetic atherosclerosis and retinal neovascularization. However, the effect of reduced β2GPI on vascular disorders in diabetic mellitus (DM) remains to be elucidated. The present study established a high glucose‑induced injury model using human umbilical cords veins (HUVECs) and evaluated the protective effects of reduced β2GPI against the injury. The data demonstrated that a low concentration of reduced β2GPI (0.5 µM) mitigated high glucose‑induced cell loss, decreased nitric oxide (NO) production and resulted in calcium overloading. Mechanically, reduced β2GPI additionally reversed high glucose‑induced phosphatase and tensin homolog (PTEN) accumulation, decrease of protein kinase B phosphorylation and nitric oxide synthase activity, and increase of cyclooxygenase‑2 activity. It was further confirmed that PTEN inhibitor‑bpV (1 µM) exhibited similar effects to those resulting from reduced β2GPI. Overall, the data revealed that reduced β2GPI exerts protective effects from glucose‑induced injury in HUVECs, potentially via decreasing PTEN levels. The present study suggests reduced β2GPI may act as a novel therapeutic strategy for the treatment of vascular disorders in DM.