2010•Zhongguo bijiao yixue zazhiRequires access

Establishment of the Rabbit Model of Chronic Renal Failure

Li Zian

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Abstract

Objective To establish the rabbit model of chronic renal failure by unilateral ureteral obstruction (UUO). Then to prove renal tubulointerstitial fibrosis can be induced ideally. Methods Normal rabbits were randomly divided into normal control group and UUO group. Detecting blood biochemical indicators of renal function at each time point,and pathological changes in the renal interstitial,monitoring of glomerular filtration rate by SPECT. Analysis of the expression of TGF-β1 showed by immunohistochemistry. Results UUO after the first 2 weeks,Scr increased and BUN did not change significantly. At 8 weeks Scr and BUN increased ( P 0. 01). The first 4 weeks as early as during the performance of interstitial fibrosis,at 8 weeks glomerular sclerosis began to appear and interstitial fibrosis increased (P 0. 05). The first 4 weeks of GFR in UUO group lower than the normal group,to the first 8 weeks of GFR in UUO decreased significantly and glomerular filtration function was lost. Immunohisto-chemistry showed that TGF-β1 had a scanty expression in the normal group. The expression at 4,8 and 12 weeks had a significant increase (P 0. 05). Conclusion UUO is a more stable model,and the first 8 weeks in UUO group would be an ideal time of renal interstitial fibrosis in animal model.

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Objective To establish the rabbit model of chronic renal failure by unilateral ureteral obstruction (UUO). Then to prove renal tubulointerstitial fibrosis can be induced ideally. Methods Normal rabbits were randomly divided into normal control group and UUO group. Detecting blood biochemical indicators of renal function at each time point,and pathological changes in the renal interstitial,monitoring of glomerular filtration rate by SPECT. Analysis of the expression of TGF-β1 showed by immunohistochemistry. Results UUO after the first 2 weeks,Scr increased and BUN did not change significantly. At 8 weeks Scr and BUN increased ( P 0. 01). The first 4 weeks as early as during the performance of interstitial fibrosis,at 8 weeks glomerular sclerosis began to appear and interstitial fibrosis increased (P 0. 05). The first 4 weeks of GFR in UUO group lower than the normal group,to the first 8 weeks of GFR in UUO decreased significantly and glomerular filtration function was lost. Immunohisto-chemistry showed that TGF-β1 had a scanty expression in the normal group. The expression at 4,8 and 12 weeks had a significant increase (P 0. 05). Conclusion UUO is a more stable model,and the first 8 weeks in UUO group would be an ideal time of renal interstitial fibrosis in animal model.

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Available abstract

Objective To establish the rabbit model of chronic renal failure by unilateral ureteral obstruction (UUO). Then to prove renal tubulointerstitial fibrosis can be induced ideally. Methods Normal rabbits were randomly divided into normal control group and UUO group. Detecting blood biochemical indicators of renal function at each time point,and pathological changes in the renal interstitial,monitoring of glomerular filtration rate by SPECT. Analysis of the expression of TGF-β1 showed by immunohistochemistry. Results UUO after the first 2 weeks,Scr increased and BUN did not change significantly. At 8 weeks Scr and BUN increased ( P 0. 01). The first 4 weeks as early as during the performance of interstitial fibrosis,at 8 weeks glomerular sclerosis began to appear and interstitial fibrosis increased (P 0. 05). The first 4 weeks of GFR in UUO group lower than the normal group,to the first 8 weeks of GFR in UUO decreased significantly and glomerular filtration function was lost. Immunohisto-chemistry showed that TGF-β1 had a scanty expression in the normal group. The expression at 4,8 and 12 weeks had a significant increase (P 0. 05). Conclusion UUO is a more stable model,and the first 8 weeks in UUO group would be an ideal time of renal interstitial fibrosis in animal model.

Key concepts: Renal function, Medicine, Urology, Pathological, Fibrosis, Immunohistochemistry, Chronic renal failure, Internal medicine

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