The pathogenesis of diabetic retinopathy is characterized by retinal edema, hemorrhage, ischemia, increased neovascularization and neuronal degeneration in the retina, which leads to microvascular breakdown of the blood-retinal barrier, and results in retinal hemorrhage and edema. In an in vivo study, STZ-diabetic rats were given puerarin (80 mg/kg/d, i.p.) before and after administration of STZ(60mg/kg, i.p.). Puerarin significantly ameliorated the retinopathy progression and the increases BEGF and HIF-1 mRNA expression in the retina of STZ diabetic rats after 3 months of intervention (Teng et al., 2009). in another study, the protective effect of puerarin on ocular hypertension and ischemia was investigated. Puerarin(1%, w/v, 50μL) noticeably decreased the choroidal and ciliary body blood flow as compared to control. In addition, administration of puerarin (10mg/kg, i.p.) immediately prior to the onset of surgically-induced ocular ischemia significantly improved byt indicated that puerarin facilitates retinal function recovery, primarily via increase of chorodial ciliary body blood flow.

Protection of diabetic vascular dysfunction

It is well accepted that diabetes is associated with abnormalities of the endothelial function, which increases the risk of the development of CVD and cerebral vascular diseases in diabetic patients (Vanhoutte et al., 2009; Ding and Triggle, 2010). Pre-treatment of puerarin (100 μmol/L) before high glucose intervention significantly inhibited VSMC proliferation, ROS and nicotinamide adenine dinucleotide phosphate(NADPH) oxidase activity in VSMCs of rats. Indeed, puerarin attenuated the high glucose-induced phosphorylation and membrane translocation of PKCβ2, Rac1, p47phox and p67phox subunits. Similar results were observed when obese Zucker rats were given puerarin (100 mg/kg/d, i.g.) for 2 weeks before and after carotid arterial balloon injury.

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