Suppressive Effects of Ursolic Acid on Human Endometriotic Stromal Cells Survival

article OA: closed CC0 ⤵ 7 in-corpus citations
View on OpenAlex View on PubMed View at publisher
AI-generated summary by gemini-2.5-flash-lite, 2026-06-06

Ursolic acid reduced the survival of human endometriotic stromal cells by inhibiting proliferation and angiogenesis and promoting apoptosis, while decreasing COX-2 expression and PGE2 production.

One-sentence paraphrase of the abstract; not a substitute for reading it. No clinical advice. How this works

Abstract

BACKGROUND/AIMS: The identification of new compound candidates for endometriosis treatment is needed. Cyclooxygenase-2 (COX-2) is considered a crucial target to control the progress and recurrence of endometriosis. Here, we identified ursolic acid (UA) as a natural inhibitor of COX-2 and investigated its effects on endometriosis progression. METHODS: Primary human endometriotic stromal cells isolated from patients with endometriosis were exposed to UA at concentrations of 15, 30, 45, and 60 μM. 3-(4,5-Dimethylthiaziazol-2-yl)-2,5-diphenyl tetrazolium bromide assays, 5'-bromo-2'-deoxy-uridine assays, and Caspase-3 activity measurements were performed to detect cell growth and apoptosis. Enzyme-linked immunosorbent assays were used to detect COX-2 and vascular endothelial growth factor (VEGF) protein expression and prostaglandin E2 (PGE2) levels. Capillary-tubule formation assays using human umbilical vein endothelial cells were also carried out to determine angiogenesis. RESULTS: UA significantly decreased cell viability, inhibited proliferation, and increased caspase-3 activity in a dose-dependent manner. COX-2 protein expression and the subsequent PGE2 production were both reduced by UA. Meanwhile, UA exposure decreased VEGF secretion in the stromal cells and the capillary-tubule formation assay confirmed the inhibitory effect of UA on angiogenesis. Furthermore, UA increased the phosphorylation of c-Jun N-terminal kinase and p38. CONCLUSIONS: Our data suggest that UA plays a role as a natural inhibitor of COX-2 to control the survival of human endometriotic stromal cells by inhibiting proliferation and angiogenesis and promoting apoptosis.

My notes (saved in your browser only)

Condition tags

endometriosis

MeSH descriptors

Cyclooxygenase Inhibitors Endometriosis Endometrium Neovascularization, Pathologic Triterpenes Apoptosis Apoptosis Cell Proliferation Cell Proliferation Cell Survival Cell Survival Cyclooxygenase 2 Cyclooxygenase 2 Cyclooxygenase Inhibitors Dinoprostone Dinoprostone Endometriosis Endometriosis Endometrium Female

Citation neighborhood

Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.

References (53)

Cited by (7)

Source provenance

europepmc
last seen: 2026-08-14T06:11:53.302379+00:00
openalex
last seen: 2026-06-10T17:14:06.276822+00:00
pubmed
last seen: 2026-05-13T22:22:35.348889+00:00
License: CC0 · commercial use OK