Effect of Biochanin A on Retina Levels of Vascular Endothelial Growth Factor, Tumor Necrosis Factor-Alpha and Interleukin-1Beta in Rats With Streptozotocin-Induced Diabetes

Objectives: Without proper medication for the treatment of diabetic retinopathy, retinal cells become malnourished and degenerate, which results in damage to vision cells and can lead to blindness. Flavonoids such as biochanin A (BCA) can directly target various facets of angiogenesis. We assessed the effect of administrating BCA on angiogenic and inflammatory markers in the retina of rats with diabetes.

Methods: We randomly selected 2 groups from 30 male Wistar rats. We used 6 rats in each group. We selected 1 control group, Group 1 (which received 0.5% dimethyl sulfoxide), and a second group, Group 2, which received 10 mg/kg body weight (bw) of BCA. Type 1 diabetes was induced in other rats by a single injection of streptozotocin (55 mg/kg bw). Rats with diabetes were randomly divided into 3 groups as follows: Group 3, the control group with diabetes, which received 0.5% dimethyl sulfoxide; and Groups 4 and 5, which received 10 and 15 mg/kg bw of BCA, respectively. The concentration of vascular endothelial growth factor, tumor necrosis factor-alpha and interleukin-1beta were quantified in the retina of rats with diabetes that received BCA for 6 weeks, and the levels were compared to those of control rats.

Results: Administration of BCA to rats with diabetes resulted in a significant restoration of fasting blood glucose levels. After administration of BCA, retina concentrations of vascular endothelial growth factor, tumor necrosis factor-alpha and interleukin-1beta decreased in the 2 groups of treated rats with diabetes compared to the control group with diabetes (p<0.05). No significant difference was shown between the 2 doses of BCA.

Conclusions: Administration of BCA can improve and postpone retinopathy by lowering blood sugar, suppressing inflammation via decreasing tumor necrosis factor-alpha and interleukin-1beta, and reducing angiogenesis via decreasing vascular endothelial growth factor in the retinal tissues.