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目的研究氯化钴(CoCl2)干预条件下糖尿病(diabetes mellitus,DM)大鼠肾组织缺氧诱导因子1α(hypoxia inducible factor-1α,HIF-1α)的表达及意义。方法按数字随机化原则取8只为正常对照组(CTL组),16只为模型组,建立糖尿病肾病大鼠模型,并随机均分为糖尿病组(DM组)和CoCl2治疗组(CoCl2组)。检测相关生化指标,免疫组化学检测实验大鼠HIF-1α表达和分布,蛋白免疫印迹法(Western Blotting)检测肾脏组织HIF-1α蛋白表达。结果CTL组肾脏组织无HIF-1α表达,DM组HIF-1α主要分布于肾小管上皮细胞的胞浆和胞核;CoCl2组HIF-1α平均光密度显著高于DM组(P<0.05),其HIF-1α蛋白表达水平较DM组显著增加(P<0.05)。结论缺氧参与糖尿病肾脏疾病(diabetic kidney disease,DKD)早期肾小管间质损伤,化学性低氧模拟剂CoCl2可通过上调HIF-α减轻蛋白尿和肾小管间质损伤,延缓DKD进展。
Objective To study the expression and significance of hypoxia inducible factor-1α (HIF-1α) in the kidney of diabetic mellitus (DM) rats exposed to cobalt chloride (CoCl2). Methods According to the principle of digital randomization, 8 rats were randomly divided into diabetic group (DM group) and CoCl2 treatment group (CoCl2 group), 8 normal control group (CTL group) and 16 model group. . The related biochemical indexes were detected. The expression and distribution of HIF-1α in experimental rats were detected by immunohistochemistry. The protein expression of HIF-1α in kidney was detected by Western Blotting. Results There was no expression of HIF-1α in kidney of CTL group. HIF-1α of DM group was mainly distributed in cytoplasm and nucleus of renal tubular epithelial cells. The average optical density of HIF-1α in CoCl2 group was significantly higher than that in DM group (P <0.05) HIF-1αprotein expression was significantly higher than DM group (P <0.05). Conclusions Hypoxia is involved in the early tubulointerstitial injury of diabetic kidney disease (DKD). The chemical hypoxia-simulator CoCl2 can reduce the proteinuria and tubulointerstitial injury by increasing HIF-α, and delay the progression of DKD.