Background: Hyperglycemia contributes to a cascade of inflammatory response mechanisms in kidneys that result in the development of renal hypoxia and angiogenesis with subsequent chronic renal failure. Under a certain degree of hyperglycemia, the kidney possesses self-protection mechanisms through adaptation to hyperglycemia and hypoxia. As the hypoxia-inducible factor-1α (HIF-1α)/vascular endothelial growth factor (VEGF) axis is a key pathway for neovascularization, the inhibition of this axis is a target for renal angiogenesis therapy. Methods: Male Sprague–Dawley rats were exposed to hyperglycemia and subdivided into four groups, namely groups 1, 2, 3 and 4. Renal tissue samples were processed and analyzed to determine pathological and morphological changes, the gene expression of HIF-1α, VEGF, inflammation factor and effect of treatment. Results: We found that with hyperglycemia, HIF1α and VEGF expression were increased, inflammatory mediator IL-6 increased and vascular changes in the kidney tissues are severe in diabetic group. In contrast, the changes are minimal in the treated group. The expression of HIF-1α increased as well as the expression of VEGF, but VEGF expression in group 3 was the lowest. Group 3 had lower levels of IL-6, and least vascular changes. The results revealed that PB treatment suppressed the development of angiogenesis and DN. Conclusion: These findings suggest that affecting the HIF-1α/VEGF signaling pathway to regulate angiogenesis after infliction of hyperglycemic kidney injury may provide clues for the development of novel CKD treatments.