【摘要】 目的 探究Periostin对子宫内膜基质细胞(ESCs)增殖和血管生成的影响及其潜在的分子机制。方法 选取2019年1月至2021年1月衡水市人民医院的女性患者为研究对象，收集其子宫内膜组织，采用qRT-PCR、Western blot和免疫组化检测临床样本子宫内膜组织中Periostin mRNA和蛋白的表达。从子宫内膜组织中分离出子宫内膜基质细胞(ESCs),并通过CCK-8、EdU、Transwell分析、血管形成等实验来分析Periostin异常表达对ESCs和人脐静脉内皮细胞(HUVECs)的作用。Western blot检测PI3K/AKT/mTOR通路相关蛋白和血管内皮生长因子A(vascular endothelial growth factor A,VEGFA)的表达。用PI3K/AKT/mTOR通路抑制剂(LY294002)转染ESCs,确定PI3K/AKT/mTOR通路对子宫内膜异位症内膜基质细胞增殖和血管生成的作用。结果 异位子宫内膜组织中Periostin表达上调，Periostin促进了ESCs的增殖、迁移和侵袭，并促进了HUVECs的血管生成。此外，Periostin激活了PI3K/AKT/mTOR通路，经过LY294002处理后，过表达的Periostin对ESCs和HUVECs的促进作用减弱。结论 Periostin能通过激活PI3K/AKT/mTOR通路来促进子宫内膜异位症的进展和血管生成，这可能为子宫内膜异位症提供有前景的治疗靶点。更多还原

【Abstract】 Objective To explore the effect of Periostin on endometrial stromal cells(ESCs) proliferation and angiogenesis and its potential molecular mechanism. Methods Female patients from January 2019 to January 2021 in Hengshui People′s Hospital were selected as the research objects, and their endometrial tissues were collected. The expression of Periostin mRNA and protein in endometrial tissues of clinical samples was detected by qRT-PCR, Western blot and immunohistochemistry.ESCs were isolated from the endometrial tissues, and the effect of Periostin abnormal expression on ESCs and human umbilical vein endothelial cells(HUVECs) was analyzed by CCK-8, EdU, Transwell analysis and angiogenesis tests. The expressions of PI3K/AKT/mTOR pathway related proteins and vascular endothelial growth factor A(VEGFA) were detected by Western blot. PI3K/AKT/mTOR pathway inhibitor(LY294002) was used to transfect ESCs to determine the role of PI3K/AKT/mTOR pathway in endometrium stromal cell proliferation and angiogenesis in endometriosis. Results The expression of Periostin was up-regulated in ectopic endometrial tissues. Periostin promoted the proliferation, migration and invasion of ESCs, and promoted the angiogenesis of HUVECs. In addition, Periostin activated the PI3K/AKT/mTOR pathway. After treatment with LY294002, the promoting effect of overexpressed Periostin on ESCs and HUVECs was weakened. Conclusion Periostin promotes endometriosis progression and angiogenesis by activating the PI3K/AKT/mTOR pathway, which may provide promising therapeutic targets for endometriosis.更多还原