肾苏合剂对腺嘌呤所致大鼠肾间质纤维化影响的实验研究

Influence of Shensu Heji on Renal Interstitial Fibrosis of Rats Caused by Adenine

目的:观察肾苏合剂对大鼠肾间质纤维化生化指标、病理形态学及血管活性物质AngⅡ、ET-1的影响。方法:采用腺嘌呤灌胃法建立大鼠肾间质纤维化模型,将实验动物随机分为正常组、中药组(肾苏合剂)、西药组(苯那普利)和模型组。于造模后及治疗3、6周分别检测血清BUN、Scr、TP、ALB和24hTP、NAG、GAL。实验6周末采用光镜和电镜分别观察各组大鼠肾脏病理形态学及肾脏超微结构变化;采用放免法检测血管活性物质AngⅡ和ET-1。结果:①中药组血清BUN、Scr、24hTP、NAG、GAL等指标明显改善(P<0.05)。其中,在降低血清BUN、SCr方面,中药组优于西药组(P<0.05)。②光镜与电镜均显示,中药组大鼠肾小管损害及肾间质纤维化程度均明显减轻,西药组与中药组病理改变基本相同。③中药组肾组织中AngⅡ、ET-1的浓度明显降低(P<0.05)。结论:肾苏合剂能明显减轻腺嘌呤大鼠模型肾小管间质病理损害,阻抑肾间质纤维化的进展。

Objective：To observe the influence of Shensu Heji on the biochemical index of rat＇s renal interstitial fibrosis,pathologic morphology and vessel active mass AngⅡ and ET-1.Methods：The model rats of renal interstitial fibrosis were built by the adenine stomach-perfusion method.The experimental rats were randomly divided into normal group,Chinese drug group（Shensu Heji）,Western medicine group（Benazepril） and model group.Three and six weeks after the models were made,BUN,Scr,TP,ALB of blood serum and 24 h TP,NAG,GAL were respectively detected.When the experiment had lasted for 6 weeks,the changes of pathological morphology and renal ultromicroconstruction were respectively observed by optional and electron microscopes Vessel active mass AndⅡ and ET-1 were detected by radio-immunity.Results：1.The indes of Chinese drugs group were apparently improved（P〈0.05）,such as BUN ,Scr,24h TP,NAG,GAL of blood serum and so on.And in the aspects of decreasing BUN,Scr of blood serum ,Chinese drug group was better than that of the Westm medicine group（P〈0.050.2.Both the optional and the electron microsoopes showed that in Chinese drug group,the degrees of renal trbules＇ damage and renal interstitial fibrosis were obviously released .The pathologic changes of Chinese drug grop and Western medicine group were primarily similar.3.The consistency of AngⅡ and ET-1 in renal tissues were significantly reduced （P〈0.05）.Conclusion：Shensu Heji can apparently reduce the pathologic changes of the renal tubule＇ interstitial of model rats caused by Adenine and restrain the development of intrstitial fibroses.