Department of Obstetrics and Gynecology, Tongji Hospital of Tongji University, School of Medicine, Tongji University, Shanghai, 200065, China.
Department of Obstetrics and Gynecology, Chengdu Women's and Children's Central Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, 610000, China.
J Mater Sci Mater Med. 2024 Jul 29;35(1):39. doi: 10.1007/s10856-024-06807-w.
The process of endometrial repair after injury involves the synergistic action of various cells including immune cells and stem cells. In this study, after combing Fibrinogen(Fg) with poly(L-lacticacid)-co-poly(ε-caprolactone)(P(LLA-CL)) by electrospinning, we placed Fg/P(LLA-CL) into the uterine cavity of endometrium-injured rats, and bioinformatic analysis revealed that Fg/P(LLA-CL) may affect inflammatory response and stem cell biological behavior. Therefore, we verified that Fg/P(LLA-CL) could inhibit the lipopolysaccharide (LPS)-stimulated macrophages from switching to the pro-inflammatory M1 phenotype in vitro. Moreover, in the rat model of endometrial injury, Fg/P(LLA-CL) effectively promoted the polarization of macrophages towards the anti-inflammatory M2 phenotype and enhanced the presence of mesenchymal stem cells at the injury site. Overall, Fg/P(LLA-CL) exhibits significant influence on macrophage polarization and stem cell behavior in endometrial injury, justifying further exploration for potential therapeutic applications in endometrial and other tissue injuries.
在损伤后子宫内膜修复的过程中,涉及多种细胞的协同作用,包括免疫细胞和干细胞。在这项研究中,我们通过静电纺丝将纤维蛋白原(Fg)与聚(L-乳酸)-共-聚(ε-己内酯)(P(LLA-CL))结合,然后将 Fg/P(LLA-CL)放入子宫内膜损伤的大鼠子宫腔中,生物信息学分析表明 Fg/P(LLA-CL)可能影响炎症反应和干细胞的生物学行为。因此,我们验证了 Fg/P(LLA-CL)可以抑制脂多糖(LPS)刺激的巨噬细胞向促炎 M1 表型转化。此外,在子宫内膜损伤的大鼠模型中,Fg/P(LLA-CL)有效地促进了巨噬细胞向抗炎 M2 表型的极化,并增加了损伤部位间充质干细胞的存在。总的来说,Fg/P(LLA-CL)在子宫内膜损伤中对巨噬细胞极化和干细胞行为有显著影响,为子宫内膜和其他组织损伤的潜在治疗应用提供了进一步的探索依据。