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目的:建立糖尿病性肾病(diabetic nephropathy,DN)大鼠模型,观察DN发生发展过程中大鼠肾脏相关功能及结构的变化特点。方法:二级Wistar雄性大鼠60只,体质量180~220 g,分为2组:正常对照组和模型组各30只。模型组大鼠一次性腹腔注射链脲佐菌素(STZ,65 mg/kg),正常对照组注射等量的枸橼酸缓冲溶液。在注射后第6、10、12、16和32周,分别动态监测大鼠的体质量、血糖、24 h尿蛋白和肌酐、肾脏质量及病理改变等。结果:随着病程的发展,模型组大鼠持续高血糖,体质量明显降低,24 h尿蛋白、尿蛋白/尿肌酐比值则逐渐升高,肾脏明显肥大,而且肾小球和肾小管病变在第10周开始出现,之后病变程度逐渐加重、病变范围不断扩大,表现出较为典型的DN变化特点,诸如肾小球系膜增厚、细胞外基质增生及肾小管间质损伤等。结论:STZ可成功诱导大鼠持续性高糖血症,后者的进一步发展,又可引起大鼠肾脏功能受损和形态改变。高糖血症持续12周后,DN大鼠模型的明显特征开始显现。
OBJECTIVE: To establish a rat model of diabetic nephropathy (DN) and observe the changes of renal function and structure during the development and progression of DN. Methods: Sixty Wistar male rats were divided into two groups: normal control group and model group, with 30 rats in each group. Rats in the model group were injected intraperitoneally with streptozotocin (STZ, 65 mg / kg), and the normal control group was injected with the same amount of citrate buffer solution. At the 6th, 10th, 12th, 16th and 32th week after injection, the body weight, blood glucose, 24h urinary protein and creatinine, renal quality and pathological changes were dynamically monitored. Results: With the progression of disease, the rats in the model group continued to have hyperglycemia, the body weight decreased significantly, and the ratios of 24 h urinary protein, urine protein / creatinine gradually increased, and the kidneys were significantly hypertrophy. The glomerular and tubular lesions The first ten weeks began to appear, after the lesion gradually increased, the scope of the disease continues to expand, showing a more typical DN changes, such as mesangial thickening, extracellular matrix proliferation and tubulointerstitial injury. Conclusion: STZ can induce persistent hyperglycemia in rats, and the further development of the latter can lead to impaired renal function and morphological changes in rats. After 12 weeks of hyperglycemia, significant features of the DN rat model began to appear.