腹股沟疝无张力修补术中应用不可降解聚合物补片以增强腹股沟腹壁薄弱区，显著降低了传统腹股沟疝手术的复发率。但不可降解补片可致患者出现疼痛、补片感染和精索损伤等并发症。本研究将构建自体腹股沟疝血管化组织工程补片，用于无张力疝修补术以减少不可降解补片所致并发症。根据我们前期在腹壁疝和生物材料制备的研究基础，本研究将构建沉默Int6基因的慢病毒载体并稳定转染兔自体骨髓间充质干细胞(MSCs)；制备聚乳酸-羟基乙酸共聚物(PLGA)和脱细胞组织支架, 检测生物相容性、免疫性、力学和孔隙率；将沉默Int6基因的 MSCs种植到支架内体外培养；制备兔腹沟股疝模型；将自体组织工程补片体内移植、定期大体观察、取材检测；阐明沉默Int6基因的 MSCs促进补片血管化机制, 沉默Int6基因，可能通过上调缺氧诱导因子(HIF)2α而促补片血管新生；沉默Int6和Hif2α基因，可能下调HIF2α而抑制血管新生。

In order to reduce the complications such as pain，infection or sperm cord injury caused by the clinical available undegradable meshes in tension-free inguinal hernia repair. Based on previous studies about abdominal wall hernia or biomaterials preparation, we will develop a vascularized tissue-engineering inguinal hernia patch to replace the present polymer meshes so as to reduce the complications caused by the undegradable meshes. In this research, we will develop a lentiviral shRNA-Int6 expression vector; then transfect MSCs with lentiviral shRNA-Int6 vector. To prepare decellularized scaffold of various tissue sources and PLGA(PLA-PGA) scaffold, then the prepared scaffold will be analyzed for cell-compatibility, biocompatibility, immunogenic, mechanical strength and porosity; then shRNA-Int6 MSCs will be seeded into the preferred decellularized scaffold and PLGA scaffold respectively, then undergo dynamic and static culture in vitro. To prepare inguinal hernia model.The prepared tissue-engineering inguinal hernia patches will be implanted to the animal inguinal hernia models; at intervals, regular checking, samples collection and examinations including incision infection, histology, implanted cells tracing and spermatic cord function or structure will be performed. To explore the mechanism that shRNA-INT6 MSCs promote vascularization of the tissue-engineering inguinal hernia patch; the possible way is that the silence of Int6 of MSCs can improve the expression of Hif2α and angiogenic factors which facilitate the vascularization of the prepared patches; while the silence of double genes of Int6 and Hif2α will inhibit the expression of Hif2α and angiogenic factors and decrease the vascularization.