新发现FIP200/自噬通路正向调控成骨、成神经及血管生成，可能作为牙髓再生的理想“扳机点”。EGCG (Epigallocatechin-3-gallate)作为茶叶中的一种主要多酚化合物，可强效激活自噬通路。我们前期研究发现，单纯负载SDF-1α的丝素蛋白支架可激活自噬并诱导牙髓样组织生成；但仍存在细胞因子用量大、缺乏神经支配及再生成功率低等问题。本课题提出“EGCG协同SDF-1α激活FIP200/自噬通路促进牙髓再生”的新假设，拟通过基因转染技术过表达和沉默牙髓干细胞中FIP200，研究FIP200/自噬通路对牙髓干细胞生物学行为的影响；制备EGCG/SDF-1α双释-丝素蛋白支架，应用裸鼠皮下牙根移植模型、犬成熟恒牙根管模型等，探讨EGCG协同SDF-1α激活FIP200/自噬通路促进牙髓再生的潜在效应和机制。本系列研究利于深入了解牙髓再生的机制，并为牙髓再生的实现提供新的思路。

It is newly discovered that the FIP200/autophagy pathway positively regulates osteoblastic, neurogenic, and angiogenic process, thus arises as a promising trigger strategy for pulp regeneration. Evidence has indicated that epigallocatechin-3-gallate (EGCG), the main tea-derived polyphenol, powerfully activates the autophagy pathway. Our recent findings indicate that SDF-1α-loaded silk fibroin scaffold enhances autophagy and induces pulp-like tissue formation ectopically and in situ. However, there still remain several main concerns including high cytokine consumption, lack of innervations, and low success rate. Therefore, this project aims to comprehensively investigate the potential cooperative action of EGCG with SDF-1α activating FIP200/autophagy to facilitate pulp regeneration. Thus the thesis is devided into two parts: Part one is to determine the exact role of FIP200/autophagy pathway during biological behaviors of dental pulp stem cells by overexpression and siRNA knockdown of FIP200. Part two is to fabricate EGCG/SDF-1α dual loading silk fibroin scaffold, and investigate its pulp regenerative potential through nude mice transplantation model ectopically and canine mature root canal model in situ. Therefore, the present project may deepen molecular understanding and provide novel perspective of pulp regeneration.