Deficiency of hypoxia inducible factor‑1α promoted progression of diabetic nephropathy with hypertension

Abstract

The present study was designed to investigate the effect of hypoxia inducible factor‑1α (HIF‑1α) on diabetic nephropathy (DN) with hypertension. HIF‑1α deficient mice (Mx/HIF‑1α‑/‑) were constructed and treated with streptozotocin (STZ) injection for hypertensive DN induction. Normal C57BL/6 mice received STZ or no treatment (normal) were considered as controls. Three days post STZ administration; body weight, fasting blood glucose (FBG), 24 h urinary albumin and systolic blood pressure (SBP) were measured weekly. Periodic acid‑Schiff's staining was performed for histologic analysis of glomeruli damage. In comparison with the normal control, significant upregulation and downregulation of HIF‑1α was, respectively, detected in diabetic and HIF‑1α‑/‑ mice (P<0.01). In comparison with STZ‑induced diabetic mice, HIF‑1α‑/‑ + STZ mice displayed reduced body weight, and increased FBG, urinary albumin and SBP. PAS showed HIF‑1α‑/‑ + STZ mice had damaged kidney tissues, with more renal fibrosis and apparent glomerular hypertrophy. These results demonstrated that HIF‑1α deficiency accelerated DN progression with increasing hypertension in mice.