〔Abstract〕 Objective To investigate the effect of interfering with long noncoding RNA（LncRNA）small nucleolar RNA host gene 16（SNHG16）on improving angiogenesis of ectopic endometrial stromal cells（EScs）in adenomyosis（AM）by targeting upregulation of miRNA（miR）-141-3p and inhibition of high mobility group box-1 protein （HMGB1）. Methods The expression levels of SNHG 16，miR-141-3p and HMGB 1 mRNA in endometrial tissues of 52 patients with adenomyosis（AM group）and 52 patients who needed hysterectomy due to cervical cancer or ovarian cancer（control group）were detected by quantitative reverse transcription polymerase chain reaction（qRT- PCR）. Y 14 cells were divided into small hairpin RNA（shRNA）NC group，shRNA SNHG 16 group，shRNA SNHG 16+miR-141-3p inhibitor（inhibitor）group，shRNA SNHG 16+inhibitor NC group and blank group. The tar_ geting relationship between miR-141-3p and SNHG 16 as well as HMGB 1 was verified. The expression levels of SNHG 16，miR-141-3p and HMGB 1 mRNA in Y 14 cells were detected by qRT-PCR. Cell counting assay（CCK-8） and Transwell assay were used to detect cell proliferation，invasion and migration. Microvascular density（MVD） was determined by immunofluorescence. The expressions of hypoxia-inducing factor α（HIF-1α), cyclooxygenase- 2（Cox-2），vascular endothelial growth factor（VEGF）and HMGB 1 were detected by Western blot. Results The expression of SNHG 16 and HMGB 1 mRNA in AM group was higher than that in control group，but the expression of miR-141-3p was lower than that in control group（P<0. 05）. The expression of SNHG 16，HMGB 1 mRNA，proliferation rate，migration，invasion number，MVD，expression of VEGF，HIF-1 α , Cox-2，and HMGB 1 proteins in the shRNA SNHG 16 group were lower than those in the blank group and shRNA NC group，while the expression of miR-141-3p was higher than that in the blank group and shRNA NC group（P<0. 05）. Inhibition of miR-141-3p reversed the improvement of EScs angiogenesis by interfering with SNHG 16. Conclusion Interference with LncRNA SNHG 16 improves EScs angiogenesis and inhibits proliferation，migration，and invasion of EScs by targeting upregulation of miR-141-3p and inhibition of HMGB 1.