传出细胞增多
子宫内膜异位症
炎症
吞噬作用
病变
细胞凋亡
间质细胞
医学
巨噬细胞
癌症研究
病理
内科学
免疫学
生物
体外
生物化学
作者
Qinkun Sun,Yi‐Hong Lei,Huaying Zhang,Xinyu Ding,Mengjie Yang,Teng Zhang,Jiahao Chen,Huang Zhixiong,Lemeng Wang,Jianfa Lan,Qiansheng Huang,Qionghua Chen
标识
DOI:10.1016/j.colsurfb.2022.112893
摘要
Endometriosis is an inflammation-dependent disorder characterized by the abnormal growth of endometrium-like lesions. In recent years, there is a great deal of interest in the development of anti-inflammatory therapy. Herein, an acid-sensitive calcium carbonate nanoparticle (CaNP) incorporated BML-111 (BML@CaNP) was prepared. BML@CaNP acted as a Ca2+ nanomodulator for efferocytosis (macrophages engulf apoptotic cells). Specifically, BML@CaNP induced the apoptosis of endometriotic stromal cells and enhanced the efferocytosis of macrophages. In addition, the particle can also deliver BML to the ectopic lesion for resolving the inflammatory response. In vivo BML@CaNP effectively suppressed lesion growth in endometriosis mice model, which could be attributed to the enhancing efferocytosis of cells and the lower levels of inflammatory factors in peritoneal fluid. In addition, these nanoparticles did not show side effects. In all, we provide a new anti-inflammatory strategy by both enhancing efferocytosis and resolving inflammation for the treatment of endometriosis.
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