糖尿病膀胱病变（DCP）是糖尿病引起的泌尿系统并发症之一，我们前期研究证实高糖环境可引起膀胱Cajal 间质细胞(ICC)数量减少,形态改变，起搏和神经信号传导功能降低，进而引起膀胱逼尿肌兴奋和收缩功能下降，导致DCP，而通过构建SCL基因重组腺病毒载体，采用 SCL基因转染上调c-kit，显著改善了体外高糖环境下培养的已受损害的ICC形态和功能。为了观察经膀胱灌注进行SCL基因转染对在体DCP膀胱中 ICC表型、形态、功能损害的重塑作用及治疗DCP的可行性及有效性，本研究拟构建SCL基因重组慢病毒载体，评估慢病毒载体的体外转染效率及安全性后，经尿道将SCL基因慢病毒载体灌注入DCP膀胱，通过尿流动力学和肌条实验检测膀胱功能恢复情况，并进一步通过免疫组化、细胞膜片钳、电镜、RT-PCR、Western-blot等技术观察ICC表型及形态、功能重塑情况，从而为DCP的临床治疗探索一条新途径。

Diabetic cystopathy (DCP) is a complication of diabetes in urinary system. We previously demonstrated that high glucose can reduce the number of the interstitial cells of Cajal (ICC) in bladder and the pacing and signal-transducting function of ICC. The result was related to the decrease of detrusor function, resulting in DCP. We further demonstrated gene transfection of SCL can promote c-kit and restore redifferentiated ICC in vitro. So we want to investigate whether gene transfection of SCL can also restore redifferentiated ICC and detrusor function of DCP in vivo. At first, this study is designed to assess the efficiency and safety of SCL gene lentiviral vector after it constructed successfully. Then , we will fill SCL gene lentiviral vector into bladders of the DCP animal models through urethras. Bladder function will be tested by urodynamic and accessed by contraction of detrusor strips. Phenotype and function of ICC will further tested by immunohistochemistry , cell patch clamp, RT-PCR、Western-blot and other assays.