糖尿病膀胱病变（DCP）是糖尿病常见并发症之一，我们前期研究证实经尿道灌注SCL慢病毒，显著改善了糖尿病豚鼠DCP膀胱功能，但并不能完全逆转或者恢复受损的DCP膀胱的功能。近年来，本课题组及其他学者对缝隙连接蛋白的研究为DCP发病机制的阐明及其治疗提供了新的切入点。本课题组前期研究豚鼠DCP膀胱时在电镜下发现Cajal 样间质细胞与其他细胞间的缝隙连接显著减少、结构破坏、连接松散。因此，我们推测，在膀胱“ICC网络”兴奋传递过程中缝隙连接蛋白的异常在DCP的发病过程中可能也扮演重要角色。为观察DCP膀胱中Cx43如何分布以及Cx43和 ICC基因重组慢病毒协同治疗作用，本研究拟建立DCP豚鼠动物模型，通过肌条和尿动检测膀胱功能恢复情况，并通过免疫组化、细胞膜片钳、电镜、RT-PCR、Western-bl ot 等技术观察Cx43的数量功能恢复情况，旨在为临床治疗DCP膀胱提供新的思路。

Diabetic cystopathy (DCP) is one of the most common complications of diabetes. Our previous studies confirmed that SCL injection of lentivirus through urethra significantly improved the function of DCP bladder in diabetic guinea pigs, but it could not completely reverse or restore the function of damaged DCP bladder. In recent years, the study of connexins by our group and other scholars has provided new starting point for the elucidation of the pathogenesis of DCP and its treatment. In the previous study of the guinea pig DCP bladder, it is found by our group that gap junctions between interstitial cells of Cajal-like and other cells were significantly reduced, and structural destruction and loose connections were observed under the electron microscope. Therefore, we speculated that the abnormality of connexins in the bladder “ICC network” may also play an important role in the pathogenesis of DCP. In order to observe the distribution of Cx43 in bladder of DCP and the synergistic therapeutic effects of Cx43 and ICC recombinant lentivirus, a DCP guinea pig animal model was established, and bladder functional recovery was detected by muscle strips test and urodynamics. Immunohistochemistry and cell patch clamp, electron microscope, rt-pcr, and western-blot were used to observe the quantitative and functional recovery of Cx43. The purpose of this study is to provide a new way of thinking for the clinical treatment of DCP bladder