当前位置：
X-MOL 学术
›
Drug Des. Dev. Ther.
›
论文详情
Our official English website, www.x-mol.net, welcomes your feedback! (Note: you will need to create a separate account there.)
Emodin Reverses the Epithelial–Mesenchymal Transition of Human Endometrial Stromal Cells by Inhibiting ILK/GSK-3β Pathway
Drug Design, Development and Therapy ( IF 4.8 ) Pub Date : 2020-09-10 , DOI: 10.2147/dddt.s262816 Qiaomei Zheng 1 , Jinhua Wang 1 , Wenwen Li 1 , Xiaoyun Chen 1 , Shaozhan Chen 1 , Lihong Chen 1
Drug Design, Development and Therapy ( IF 4.8 ) Pub Date : 2020-09-10 , DOI: 10.2147/dddt.s262816 Qiaomei Zheng 1 , Jinhua Wang 1 , Wenwen Li 1 , Xiaoyun Chen 1 , Shaozhan Chen 1 , Lihong Chen 1
Affiliation
Purpose: To explore the exact mechanism through which emodin down-regulates the migration and invasion abilities of endometrial stromal cells. Moreover, to explore the theoretical basis of emodin in the treatment of endometriosis.
Patients and Methods: Endometriosis endometrial stromal cells (EESs) were cultured from 15 women with endometriosis and control endometrial stromal cells (CESs) were cultured from 12 women without endometriosis. The levels of proteins were evaluated by Western blot. The migration and invasion abilities of cells were detected by transwell assays.
Results: The abilities of migration and invasion of EESs were much stronger than those of CESs. After treated with emodin, the migration and invasion abilities of EESs and CESs were significantly down-regulated, and the levels of integrin-linked kinase (ILK) and p-GSK-3β were statistically down-regulated in EESs. Besides that, the expression of keratin was up-regulated while the expression of vimentin, β-catenin and slug were all down-regulated by emodin in a dose- and time-dependent manner. Silencing of ILK gene in EESs also achieved the above effects, which were strengthened by emodin. Conversely, exogenous expression of ILK in CESs increased the expression of p-GSK-3β, which were abrogated by emodin. Furthermore, SB216763 increased migration and invasion abilities of CESs by facilitating the epithelial–mesenchymal transition (EMT) through up-regulating levels of p-GSK-3β, β-catenin and slug, which were also abrogated by emodin.
Conclusion: Emodin inhibits the migration and invasion abilities of human endometrial stromal cells by reversing the EMT via ILK/GSK-3β pathway. So, emodin may be considered as a promising targeted therapy for endometriosis.
Keywords: emodin, endometriosis, EMT, ILK, GSK-3β
中文翻译：
大黄素通过抑制 ILK/GSK-3β 通路逆转人子宫内膜基质细胞的上皮-间质转化
目的：探讨大黄素下调子宫内膜间质细胞迁移和侵袭能力的确切机制。此外，探讨大黄素治疗子宫内膜异位症的理论基础。
患者和方法：从 15 名患有子宫内膜异位症的女性中培养子宫内膜异位症子宫内膜基质细胞 (EES)，并从 12 名没有子宫内膜异位症的女性中培养对照子宫内膜基质细胞 (CESs)。通过蛋白质印迹评估蛋白质水平。通过transwell检测检测细胞的迁移和侵袭能力。
结果：EES的迁移和入侵能力远强于CES。大黄素处理后EESs和CESs的迁移和侵袭能力显着下调，EESs中整合素连接激酶（ILK）和p-GSK-3β的水平明显下调。此外，大黄素以剂量和时间依赖性方式上调角蛋白的表达，而波形蛋白、β-连环蛋白和slug的表达均下调。EES中ILK基因的沉默也达到了上述效果，大黄素加强了这种效果。相反，在 CES 中 ILK 的外源表达增加了 p-GSK-3β 的表达，而 p-GSK-3β 被大黄素消除了。此外，
结论：大黄素通过ILK/GSK-3β通路逆转EMT，抑制人子宫内膜基质细胞的迁移和侵袭能力。因此，大黄素可能被认为是一种很有前景的子宫内膜异位症靶向治疗药物。
关键词：大黄素，子宫内膜异位症，EMT，ILK，GSK-3β
更新日期：2020-09-10
Patients and Methods: Endometriosis endometrial stromal cells (EESs) were cultured from 15 women with endometriosis and control endometrial stromal cells (CESs) were cultured from 12 women without endometriosis. The levels of proteins were evaluated by Western blot. The migration and invasion abilities of cells were detected by transwell assays.
Results: The abilities of migration and invasion of EESs were much stronger than those of CESs. After treated with emodin, the migration and invasion abilities of EESs and CESs were significantly down-regulated, and the levels of integrin-linked kinase (ILK) and p-GSK-3β were statistically down-regulated in EESs. Besides that, the expression of keratin was up-regulated while the expression of vimentin, β-catenin and slug were all down-regulated by emodin in a dose- and time-dependent manner. Silencing of ILK gene in EESs also achieved the above effects, which were strengthened by emodin. Conversely, exogenous expression of ILK in CESs increased the expression of p-GSK-3β, which were abrogated by emodin. Furthermore, SB216763 increased migration and invasion abilities of CESs by facilitating the epithelial–mesenchymal transition (EMT) through up-regulating levels of p-GSK-3β, β-catenin and slug, which were also abrogated by emodin.
Conclusion: Emodin inhibits the migration and invasion abilities of human endometrial stromal cells by reversing the EMT via ILK/GSK-3β pathway. So, emodin may be considered as a promising targeted therapy for endometriosis.
Keywords: emodin, endometriosis, EMT, ILK, GSK-3β
中文翻译：
大黄素通过抑制 ILK/GSK-3β 通路逆转人子宫内膜基质细胞的上皮-间质转化
目的：探讨大黄素下调子宫内膜间质细胞迁移和侵袭能力的确切机制。此外，探讨大黄素治疗子宫内膜异位症的理论基础。
患者和方法：从 15 名患有子宫内膜异位症的女性中培养子宫内膜异位症子宫内膜基质细胞 (EES)，并从 12 名没有子宫内膜异位症的女性中培养对照子宫内膜基质细胞 (CESs)。通过蛋白质印迹评估蛋白质水平。通过transwell检测检测细胞的迁移和侵袭能力。
结果：EES的迁移和入侵能力远强于CES。大黄素处理后EESs和CESs的迁移和侵袭能力显着下调，EESs中整合素连接激酶（ILK）和p-GSK-3β的水平明显下调。此外，大黄素以剂量和时间依赖性方式上调角蛋白的表达，而波形蛋白、β-连环蛋白和slug的表达均下调。EES中ILK基因的沉默也达到了上述效果，大黄素加强了这种效果。相反，在 CES 中 ILK 的外源表达增加了 p-GSK-3β 的表达，而 p-GSK-3β 被大黄素消除了。此外，
结论：大黄素通过ILK/GSK-3β通路逆转EMT，抑制人子宫内膜基质细胞的迁移和侵袭能力。因此，大黄素可能被认为是一种很有前景的子宫内膜异位症靶向治疗药物。
关键词：大黄素，子宫内膜异位症，EMT，ILK，GSK-3β
京公网安备 11010802027423号