DPP-IV.

Diprotin A increases the phosphorylation of Src and vascular endothelial-cadherin (VE-cadherin) in human endothelial cells and disrupts endothelial cell-to-cell junctions, which are attenuated by CXCR4 (receptor of SDF-1α)-blocker or Src-inhibitor.

In the model of retinopathy of prematurity, Diprotin A increases not only retinal vascularity but also leakage. Additionally, in the murine diabetic retinopathy model, Diprotin A increases the phosphorylation of Src and VE-cadherin and aggravates vascular leakage in the retinas. Collectively, Diprotin A induces vascular leakage by augmenting the SDF-1α/CXCR4/Src/VE-cadherin signaling pathway.