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海洋胶原肽延缓腺嘌呤所致大鼠慢性肾功能损伤
作者姓名:Zhao HF  Zhang ZF  Li Q  Zhao M  Li Y
作者单位:1. 山西医科大学营养与食品卫生教研室
2. 北京大学公共卫生学院营养与食品卫生学系,100083
摘    要:目的 研究海洋胶原肽对腺嘌呤所致大鼠慢性肾功能损伤的影响.方法 利用腺嘌呤100 mg/kg制备大鼠慢性肾功能损伤的模型,观察海洋胶原肽1.125 g/kg以及2.25 g/kg两个剂量对慢性肾功能损伤的影响.于实验的第0、1、3、5、8、12周检测各组大鼠血清肌酐、尿素氮的水平,收集大鼠24 h的尿量,计算肌酐清除率.实验期间观察大鼠的精神状态、体重增长的改变,实验结束时对肾脏组织超微结构的改变进行观察.实验持续12周.结果 实验5、8、12周时,模型组动物血清肌酐水平明显升高(182.2±119.52)μmol/L、(308.17±88.37)μmol/L、(347.57±68.24)μmol/L],尿素氮水平也明显升高(29.20±16.48)mmol/L、(63.03±18.68)mmol/L、(95.53±24.88)mmol/L],而肌酐清除率明显降低(0.53±0.23)ml/min、(0.17±0.13)ml/min、(0.14±0.08)ml/min].海洋胶原肽2.25 g/kg干预组的血清肌酐和尿素氮水平在相应的时间点明显低于模型组大鼠血清的相应指标,而肌酐清除率则明显高于模型组5、8、12周时血清肌酐水平:(105.60±11.84)ml/min、(175.40±73.93)ml/min、(240.14±71.53)ml/min;尿素氮水平:(23.62±3.89)mmol/L、(41.90±23.78)mmol/L、(72.93±26.12)mmol/L;肌酐清除率:(0.99±0.35)ml/min、(0.45±0.28)ml/min、(0.26±0.06)ml/min].肾脏超微结构较模型组的损伤明显减轻.海洋胶原肽1.125 g/kg干预组较模型组比较也有改善趋势,但血清肌酐、尿素氮水平及肌酐清除率的变化与模型组比较,差异没有统计学意义.结论 海洋胶原肽2.25 g/kg可以延缓腺嘌呤导致的大鼠慢性肾功能损伤的进程.

关 键 词:肽类  腺嘌呤  肾功能不全  慢性  大鼠  Sprague-Dawley

Marine collagen peptide slow down the progression of chronic renal function impairment induced by adenine in rats
Zhao HF,Zhang ZF,Li Q,Zhao M,Li Y.Marine collagen peptide slow down the progression of chronic renal function impairment induced by adenine in rats[J].Chinese Journal of Preventive Medicine,2008,42(4):231-234.
Authors:Zhao Hai-feng  Zhang Zhao-feng  Li Qiong  Zhao Ming  Li Yong
Institution:Department of Food and Nutritional Hygiene, School of Public Health, Beijing University, Beijing 100083, China.
Abstract:OBJECTIVE: To investigate the effects of marine collagen peptide on adenine-induced chronic renal function impairment in rats. METHODS: Adenine suspension (100 mg/kg ) was given to Sprague-Dawley rats to made the model of renal function impairment. Marine collagen peptide 1.125 g x kg(-1) x d(-1) and 2.25 g x kg(-1) x d(-1) were administered intragastricly in two intervention groups. In addition, adenine suspension (100 mg/kg ) was given. Experiment was kept 12 weeks. Time-dependent levels of serum creatinine (Cr), urea nitrogen (BUN) and creatinine clearance rate were monitored. Kidney ultramicrostructure was checked through transmission electron microscope. RESULTS: In model group, level of serum Cr, BUN and Ccr of 5, 8, 12th week respectively were: (182.2 +/- 119.52, 308.17 +/- 88.37, 347.57 +/- 68.24; 29.20 +/- 16.48, 63.03 +/- 18.68, 95.53 +/- 24.88; 0.53 +/- 0.23, 0.17 +/- 0.13, 0.14 +/- 0.08). Serum Cr, BUN leves in marine collagen peptide 2.25 g x kg(-1) x d(-1) treated rats were lower and Ccr was higher significantly than that of model group. Level of serum Cr, BUN and Ccr of 5, 8, 12th week in marine collagen peptide treatment group respectively were: (105.60 +/- 11.84, 175.40 +/- 73.93, 240.14 +/- 71.53; 23.62 +/- 3.89, 41.90 +/- 23.78, 72.93 +/- 26.12; 0.99 +/- 0.35, 0.45 +/- 0.28, 0.26 +/- 0.06). Besides, kidney ultramicrostructure damage was ameliorated. Favorable effect of marine collagen peptide 1.125 g x kg(-1) x d(-1) was also observed on renal function impairment, but the difference compared to model group was not significant. CONCLUSION: Marine collagen peptide at a dose of 2.25 g x kg(-1) x d(-1) might slow down the progression of chronic renal function impairment induced by adenine in rats.
Keywords:Peptides  Adenine  Renal insufficiency  chronic  Rats  Sprague-Dawley
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