Protective Effects of Fufang Xueshuantong on Diabetic Retinopathy in Rats

الملخص EN

The aim of this study was to evaluate the protective effects of Fufang Xueshuantong (FXT) on diabetic retinopathy in rats induced by streptozotocin (STZ).

Diabetes was induced in Sprague-Dawley rats by a single injection of 60 mg/kg STZ.

One week after STZ, FXT 0.525 g/kg or 1.05 g/kg was administrated to the rats by intragastric gavage (ig) once daily consecutively for 24 weeks.

The control rats and untreated STZ rats received vehicle the same way.

At the end of the experiment, the erythrocyte aggregation and blood viscosity were assayed.

The retina vessel morphology was observed in retinal digestive preparations.

Expression of occludin and intercellular adhesion molecule-1 (ICAM-1) in retina was measured by western blotting.

Expression of vascular endothelial growth factor (VEGF) and pigment epithelium derived factor (PEDF) in retina was detected by immunohistochemistry.

The activity of aldose reductase in retina was investigated with a NADPH oxidation method.

The results showed that, in STZ rats, there were distinct lesions in retinal vessel, including decrease of pericytes and increase of acellular capillaries, together with dilatation of retinal veins.

The expression of VEGF and ICAM-1 increased, while the expression of PEDF and occludin decreased.

The activity of aldose reductase elevated, and the whole blood viscosity, plasma viscosity, and erythrocyte aggregation also increased after STZ stimulation.

FXT 0.525 g/kg and 1.05 g/kg demonstrated significant protective effects against STZ induced microvessel lesion in the retina with increased pericytes and reduced acellular capillaries.

FXT also reduced the expression of VEGF and ICAM-1 and enhanced the expression of PEDF and occludin in STZ insulted rats.

The activity of aldose reductase, the whole blood viscosity, plasma viscosity, and erythrocyte aggregation also decreased after FXT treatment.

The results demonstrated that FXT has protective effect on STZ induced diabetic retinopathy in rats.