Kayisli, Umit A.Berkkanoglu, MuratZhang, LufangKizilay, GulnurArici, Aydin2024-06-122024-06-1220071933-7205https://doi.org/10.1177/1933719107305865https://hdl.handle.net/20.500.14551/20813Many chemokines likely contribute to the pathogenesis of endometriosis. The authors hypothesize that the broad-spectrum chemokine inhibitor NR58-3.14.3 may prevent ectopic human endometrium implantation and growth. After placing human endometrium fragments into the peritoneal cavity, ovariectomized athymic nude mice (n = 31) receiving intramuscular estradiol valerate were randomly assigned to daily intraperitoneal injections of either phosphate-buffered saline or NR58-3.14.3. Fourteen days later, the implant number and volume, proliferating cell nuclear antigen (PCNA) and terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick end-labeling (TUNEL) index, and MTT cell viability were assessed in the implants. NR58-3.14.3 reduced the total number (45%) and total volume (81%) of endometriotic lesions (P < .05) and revealed a lower PCNA and higher TUNEL index in ectopic implants compared with controls (P < .05). NR58-3.14.3 treatment did not affect endometrial cell proliferation in vitro. NR58-3.14.3, by possibly regulating cell survival, can reduce the number and size of ectopic implants in vivo, supporting the potential use of chemokine inhibitors in novel therapies for endometriosis.en10.1177/1933719107305865info:eu-repo/semantics/closedAccessEndometriosisChemokine InhibitorsProliferationApoptosisNude MiceMonocyte Chemotactic Protein-1Endothelial Growth-FactorPeritoneal-FluidStromal CellsInfertile WomenInterleukin-8MacrophagesIdentificationProliferationTissueArticle148825835Q4WOS:0002520329000132-s2.0-3904913030318089601Q2