Pro-EGCG通过调节单核细胞-髓系来源的抑制细胞来抑制子宫内膜异位症的进展
Pro-EGCG suppresses endometriosis progression via regulating monocytic myeloid-derived suppressor cells.
摘要(中文译文)
Pro-EGCG对子宫内膜异位症显示出治疗前景，但其免疫调节机制尚不清楚。髓源性抑制细胞（MDSCs）是疾病进展的关键驱动因素。本研究探讨Pro-EGCG是否通过调节MDSC介导的免疫和基质失调来缓解子宫内膜异位症。在实验性子宫内膜异位症小鼠模型中，通过评估病灶负荷、组织学和MDSC动态变化来评价Pro-EGCG的治疗效果。通过过继转移验证了单核细胞型MDSC（M-MDSCs）的功能必要性。通过流式细胞术和多重免疫荧光染色，在患有或不患有子宫内膜异位症的女性外周血和病灶中评估了临床相关性。此外，在体外检测了Pro-EGCG对人PBMC来源M-MDSCs的直接作用，包括其免疫抑制功能及其在人子宫内膜异位基质细胞共培养体系中促进纤维化的能力。在小鼠模型中，Pro-EGCG治疗显著降低了病灶重量、体积和纤维化，同时伴有全身和局部M-MDSC的一致减少。浸润病灶的M-MDSCs而非多形核MDSCs（PMN-MDSCs）与疾病严重程度呈正相关。过继转移M-MDSCs可逆转Pro-EGCG的治疗效果。在临床样本中，数据证实与对照组相比，子宫内膜异位症患者的M-MDSCs显著扩增。在体外，Pro-EGCG通过抑制ROS、Arg-1和NO的产生，损害了人M-MDSC的存活并削弱了其抑制能力。此外，Pro-EGCG预处理消除了M-MDSC诱导的基质细胞增殖和纤维化基因表达。Pro-EGCG通过抑制M-MDSC的积聚、免疫抑制功能和促子宫内膜异位活性来阻碍子宫内膜异位症的进展。这些发现使Pro-EGCG成为子宫内膜异位症和其他M-MDSC驱动的炎症性疾病的潜在免疫治疗药物。
Abstract
Pro-EGCG has shown therapeutic promise for endometriosis, yet its immunoregulatory mechanisms remain unclear. Myeloid-derived suppressor cells (MDSCs) are key drivers of disease progression. This study investigates whether Pro-EGCG alleviates endometriosis by modulating MDSC-mediated immune and stromal dysregulation. The therapeutic effects of Pro-EGCG were evaluated in an experimental endometriosis mouse model by assessing lesion burden, histology, and MDSC dynamics. The functional necessity of monocytic MDSCs (M-MDSCs) was validated via adoptive transfer. Clinical relevance was assessed in peripheral blood and lesions from women with or without endometriosis via flow cytometry and multiplex immunofluorescence staining. Furthermore, the direct effects of Pro-EGCG on human PBMC-derived M-MDSCs were examined in vitro, including their immunosuppressive function and their ability to promote fibrosis in a co-culture system with human endometriotic stromal cells. In the mouse model, Pro-EGCG treatment significantly reduced lesion weight, volume, and fibrosis, accompanied by consistent M-MDSC reduction systemically and locally. Lesion-infiltrating M-MDSCs, rather than polymorphonuclear MDSCs (PMN-MDSCs), positively correlated with disease severity. Adoptive transfer of M-MDSCs reversed Pro-EGCG's therapeutic effects. In clinical samples, data confirmed a significant expansion of M-MDSCs in patients with endometriosis compared to controls. In vitro, Pro-EGCG compromised human M-MDSC survival and impaired their suppressive capacity by inhibiting ROS, Arg-1, and NO production. Furthermore, M-MDSC-induced stromal cell proliferation and fibrotic gene expression were abolished by Pro-EGCG preconditioning. Pro-EGCG hinders endometriosis progression by inhibiting M-MDSC accumulation, immunosuppressive functions, and pro-endometriotic activities. These findings position Pro-EGCG as a potential immunotherapy for endometriosis and other M-MDSC-driven inflammatory disorders.
如何引用
AMA
Qianhan Xu, Lu Chen, Jun Chen, Haoyue Hu, Zhihua Luo, Zhentao Gong, et al. Pro-EGCG suppresses endometriosis progression via regulating monocytic myeloid-derived suppressor cells.. Chinese medicine. 2026; doi:10.1186/s13020-026-01451-8.
APA
Qianhan Xu, Lu Chen, Jun Chen, Haoyue Hu, Zhihua Luo, Zhentao Gong, et al (2026). Pro-EGCG suppresses endometriosis progression via regulating monocytic myeloid-derived suppressor cells.. Chinese medicine. https://doi.org/10.1186/s13020-026-01451-8
GB/T 7714
Qianhan Xu, Lu Chen, Jun Chen, Haoyue Hu, Zhihua Luo, Zhentao Gong, et al. Pro-EGCG suppresses endometriosis progression via regulating monocytic myeloid-derived suppressor cells.[J]. Chinese medicine, 2026 doi:10.1186/s13020-026-01451-8.
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