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Objective: Proliferative diabetic retinopathy (PDR) is one of the main complications of diabetes, which is mainly caused by the abnormal proliferation of retinal vascular endothelial cells and the formation of new blood vessel.
Methods: Diabetic mice model of PDR was established by feeding a high-fat and high-sugar diet and intraperitoneal injection of streptozotocin (STZ, 50 mg/kg.
Simultaneously, high glucose-exposed human retinal capillary endothelial cells (HRCECs) were used to simulate PDR in vitr.
RESULTS: In vivo experiments showed that BJ inhibited the formation of acellular capillaries, decreased the expression of VEGF, and increased the level of ZO-1 in the retina of diabetic mic.
Conclusion: BJ inhibited the formation of cell-free capillaries and the instability of retinal structure in the retina of DR mice by inducing cell cycle arrest and reducing mitochondrial membrane potential, inhibited the proliferation of high glucose-exposed HRCECs, and induced apoptosis, indicating that BJ has the potential to treat D.
Source:
Liu QP, Chen YY, Yu YY, et a.