MsPGN湿热型大鼠AQP-2表达及ADH变化的实验研究

Experimental study on the change of AQP-2 and ADH of rats with damp-heat type of MsPGN

目的研究系膜增生性肾炎(MsPGN)湿热型大鼠水通道蛋白-2(AQP-2)的表达及抗利尿激素(ADH)的变化及湿热蕴郁的机制,并探讨慢肾蛋白停对其的影响及作用机理。方法采用手术摘除一侧肾脏加腹腔多次注射牛血清白蛋白(BSA)与大肠杆菌内毒素(LPS)及皮下多次注射完全弗氏佐剂,复制MsPGN湿热模型,慢肾蛋白停予以防治性治疗,测定各组肾组织和血浆AQP-2及ADH。结果模型组大鼠血浆中AQP-2含量明显降低,肾组织AQP-2灰度值和血浆ADH含量明显升高,与正常对照组比较差异有统计意义(P<0.05)。而慢肾蛋白停组、肾炎四位片组能升高血浆AQP-2含量,降低肾组织AQP-2灰度值和血浆ADH含量,与模型组比较差异均有统计意义(P<0.05)。慢肾蛋白停组降低ADH含量较肾炎四位片组显著,两组比较差异有统计意义(P<0.05)。结论AQP-2与MsPGN湿热证表现出密切的相关性。慢肾蛋白停能增加血浆与肾组织AQP-2含量,降低血浆ADH水平。

Objective To study the changes of AQP-2 and ADH of rats with damp-heat type of MsPGN and the mechanism of retention of damp-heat in the interior. Methods Damp-heat type of MsPGN models were made by cutting one side kidney and injecting BSA, LPS and complete Freund＇s adjuvant. Used Manshen Danbaiting to prevent and treat,and determined AQP-2 in kidney tissue and plasma and ADH in plasma of every group. Results Compared with normal group, plasma AQP-2 of model group was significantly decrease, and the grey of AQP-2 in kidney tissue and plasma ADH was significantly increase, there was obvious difference between 2 groups（P 〈 0.05）. Compared with model group, plasma AQP-2 of Manshen Danbaiting group and Shenyan Siweipian group was significantly increase, and the grey of AQP-2 in kidney tissue and plasma ADH was significantly decrease （P 〈 0.05）. Compared with Shenyan Siweipian group, plasma ADH in Manshen Danbaiting group was significantly decrease, there was obvious difference between 2 groups（P 〈0.05 ）. Conclusion AQP-2 is interrelated with damp-heat type of MsPGN. Manshen Danbaiting can increase the content of AQP-2 in plasma and kidney tissue, and decrease the level of ADH.