Abstract
Inflammatory stress and angiogenesis participate in diabetic retinopathy. miR-199α could inhibit the elevation of wound angiogenesis by suppressing TNF-α and NF-κB pathway. The mechanism of miR-199a in streptozotocin (STZ)-induced cell damage was assessed by ELLISA kit, western blotting, real-time RT-PCR. Reactive oxygen Species (ROS) was measured by flow cytometry. The over expression of miR-199a decreased the STZ-stimulated oxidative stress, inflammatory response, as well as VEGF expression. In conclusion, our results validated that overexpression of miR-199a protects RMECs from STZ-induced inflammation, oxidative stress and angiogenesis by targeting, at least partly, the VEGF signaling.
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