肾小管上皮细胞向间充质细胞转分化(EMT)是DN的主要病理特征，病程进展可引起终末期肾衰竭，治疗困难。研究表明，Id2表达减少参与EMT过程，而Id2又必须与bHLH转录因子结合才能发挥调节下游靶基因的作用，Twist是一种bHLH结构的转录因子，在肿瘤中Id2也可通过结合Snail发挥作用，二者均为EMT的重要调节因子，但DN中Id2对Twist、Snail的作用机制并不清楚；BMP-7可通过上调Id2水平而对抗TGF-β1/Smad2/3信号导致的EMT，但BMP-7如何调控Id2表达的机制也不清楚。前期研究发现氧化苦参碱可能通过Id2改善DN肾纤维化，但具体机制仍不清楚。基于此，本项目采用多手段进行干预，围绕Id2的上下游调控通路系统分析氧化苦参碱的保护机制，阐明其作用靶点，为苦参资源的合理利用和增加“糖尿病肾病”功能主治提供新的实验依据，促进中医药研究的治疗应用具有重要的社会意义。

Renal tubular epithelial-to-mesenchymal transition (EMT) are the main pathological changes of diabetic nephropathy (DN), which is a common cause of end-stage renal disease and treatment difficulty. Previous studies have suggested that the expression of Id2 decreased as a key role in development of EMT. And Id2 must combine with basic helix-loop-helix(bHLH) transcription factors to adjust the role of downstream target genes. Twist is a kind of the structure of the bHLH transcription factor and Id2 also can combine with Snail in the tumor diseases, both are the important regulatory factor for epithelial-to-mesenchymal transition. However, the regulating mechanisms have not been clearly clarified. BMP-7 can up-regulate the expression of Id2 against the transforming growth factor-β/ Smad2/3 signal caused by high glucose-induced EMT, but its mechanisms of regulation on the renal tubular EMT in DN are unknown. In our previous investigation, Oxymatrine may significant ameliorate renal tubular interstitial fibrosis and inhibit renal tubular EMT through Id2, but the underlying mechanisms have not clearly clarified. Based on this, this study was performed to the multiple means and around the regulation pathway of upstream and downstream of Id2 and to clarify the protection mechanisms of Oxymatrine and its targets. In further research, the focus will be on the sophora resources reasonable use and increase "diabetic nephropathy" attending to provide new experimental basis function. Furthermore, Oxymatrine could promote the research of Chinese medicine treatment application and has important social significance.