肾阳虚大鼠模型的水通道蛋白1改变

Change of aquaporin-1 in rat models of kidney-yang-deficiency syndrome

目的:探讨中医学肾阳虚证的物质基础。方法:运用腺嘌呤灌服和氢化可的松肌肉注射2种方法制备大鼠肾阳虚模型(分别称为模型Ⅰ和模型Ⅱ),100只Wistar大鼠随机分为正常对照组,模型Ⅰ组,模型Ⅱ大、中和小剂量组。造模结束后,常规生化法检测血肌酐(serum creatinine,SCr)、血尿素氮(blood urea nitrogen,BUN)、尿肌酐(urine creatinine,UCr)含量,冰点比重法检测尿渗透压(urine osmotic pressure,Uosm)、高岭土法检测尿17-羟皮质类固醇含量。实时逆转录聚合酶链式反应检测肾脏组织中水通道蛋白-1表达。结果:两种模型大鼠均出现类似肾阳虚证表现。与正常对照组和模型Ⅱ各剂量组比较,模型Ⅰ组大鼠SCr和BUN含量升高(P<0.05),UCr含量和Uosm降低(P<0.05)。模型Ⅰ组大鼠尿17-羟皮质类固醇含量和肾组织AQP-1表达比正常对照组下降(P<0.05)。与正常对照组比较,模型Ⅱ中剂量组SCr含量增加(P<0.05),尿17-羟皮质类固醇含量降低(P<0.05),而模型Ⅱ各剂量组大鼠肾组织AQP-1表达升高(P<0.05),并显示出一定的剂量依赖关系,以高剂量组升高最为明显。结论:水通道蛋白可能是肾阳虚证的物质基础之一。

Objective：To explore the material foundation of kidney-yang-deficiency syndrome.Methods：Two kinds of rat models of deficiency of kidney-yang were induced by adenine intragastric administration（model Ⅰ） and hydrocortisone intramuscular injection（model Ⅱ）.One hundred rats were randomly divided into normal control group,model Ⅰ group,low-dose model Ⅱ group,medium-dose model Ⅱ group and high-dose model Ⅱ group.After model establishment,contents of serum creatinine（SCr）,blood urea nitrogen（BUN）,and urine creatinine（UCr） were detected by automatic biochemistry analyzer;freezing point method was used for 24-hour urinary osmotic pressure（Uosm） testing and kaolinite method was used to detect the content of urinary 17-hydroxycorticosteroid（17-OHCS）.Expression of aquaporin-1 in renal tissue was observed by using real time reverse transcription polymerase chain reaction.Results：The rats of model groups had the characteristics of kidney-yang deficiency syndrome.The contents of SCr and BUN were significantly higher in model Ⅰgroup than in normal control group and three model Ⅱ groups（P〈0.05）,and UCr and Uosm were significantly lower（P〈0.05）.The level of urinary 17-OHCS and expression of aquaporin-1 in renal tissue were decreased in the model Ⅰ group（P〈0.05） as compared with the normal control group.Compared with the normal control group,the content of SCr was increased and urinary 17-OHCS was decreased in the medium-dose model Ⅱ group,but the expression of aquaporin-1 was increased in three model Ⅱ groups with a dose-dependent manner.Conclusion：Aquaporin-1 may be one of the material foundations of kidney-yang-deficiency syndrome.