腺嘌呤诱导幼鼠慢性肾功能衰竭模型建立的实验研究

Experimental study of juvenile rats with chronic renal failure induced by adeniene

目的探讨腺嘌呤灌胃法制作幼鼠慢性肾功能衰竭模型的效果。方法 4周龄雄性Wistar大鼠24只,随机分为正常组和模型组,每组12只。模型组按200 mg/(kg·d)剂量灌胃给予2%腺嘌呤混悬液,诱导幼鼠慢性肾功能衰竭模型。测定血清尿素氮、肌酐及24 h尿蛋白含量,取肾组织进行HE、PAS、Masson染色,并用JG12免疫组化观察肾小球毛细血管的变化,评价模型的制作效果。结果腺嘌呤灌胃后32 d,模型组大鼠血清尿素氮、肌酐、24 h尿蛋白含量较正常组明显增高[BUN:15.22±4.25 vs 4.52±0.94,P<0.01;SCr:198.22±84.16 vs 42.81±9.07,P<0.01;24 h尿蛋白:73.37±31.08 vs 11.61±1.04,P<0.05]。肾脏病理染色结果发现部分肾小球硬化,肾小管萎缩、坏死、脱落,肾间质纤维化,JG12染色结果显示肾小球毛细血管细胞数目减少。结论成功建立幼鼠慢性肾功能衰竭模型,血生化指标及肾脏病理损伤符合慢性肾功能衰竭病理生理学特点。

Objective To investigate the effect of adenine-induced chronic renal failure（ CRF） model in juvenile rats. Methods The 4-week-old male Wistar rats were randomly divided into normal group（ n = 12） and CRF group（ n = 12）. The 2% adenine suspension was gavaged to induce chronic renal failure in juvenile Wistar rats. The contents of urea nitrogen,creatinine in serum and 24 h urinary protein were determined. The renal tissue was taken to observe the histopathological changes by HE,PAS and Masson staining for evaluating the effect of the model. Results The serum urea nitrogen,creatinine and 24 h urinary protein levels were significantly higher in rats with adenine-induced CRF than in normal rats[BUN： 15. 22 ± 4. 25 vs 4. 52 ± 0. 94,P〈0. 01; SCr： 198. 22 ± 84. 16 vs42. 81 ± 9. 07,P〈0. 01; 24 h urinary protein： 73. 37 ± 31. 08 vs 11. 61 ± 1. 04,P〈0. 05]. HE,PAS and Masson staining of kidney showed glomerular sclerosis,renal tubular atrophy,necrosis,abscission,and renal interstitial fibrosis. Conclusion The model of chronic renal failure in juvenile rats by intragastric administration of adenine is successfully established. Blood biochemical indicators and renal pathological damage conform to pathological physiology of CRF.