Epigallocatechin Gallate and Prolactin JAK2 Related Signaling in Experimental Endometriosis An Integrated Analysis of In Vivo and In Vitro Models
Year: 2026
Type: dataset
Abstract: Objective: To evaluate the therapeutic effects of intraperitoneally administered epigallocatechin gallate (EGCG) on peritoneal endometriosis (EMs) and explore underlying molecular mechanisms, particularly the prolactin (PRL)-JAK2-mediated JNK/p38/ERK signaling cascade. Methods: In vitro CCK‑8 assays evaluated EGCG concentration-dependent cytotoxicity in 12Z cells. Cellular responses to PRL, EGCG, JAK2 inhibitor AG490, and combined EGCG+AG490 were characterized. A rat autologous peritoneal EMs model was established; treatment started at week 4 after lesion confirmation. Ectopic lesion volume, pain behaviors, histopathology and proinflammatory cytokines were measured (n=15 per group). Transcriptome sequencing, bioinformatic enrichment, Western blot and qRT‑PCR were applied to identify pathway alterations. Results: EGCG reduced cell viability concentration-dependently (53.31% at 50 μM, 7.80% at 200 μM). EGCG modulated PRL-associated molecules and apoptosis, and these effects were partially reversed by AG490. In vivo, EGCG alleviated pain behaviors and decreased IL‑1β, IL‑6 and TNF‑α. Median lesion volumes were 31.08 mm³ (EGCG) vs 42.88 mm³ (model), without statistical significance after Dunn‑Bonferroni correction. Transcriptomics revealed DEGs enriched in PRL, inflammatory and oxidative stress pathways. EGCG elevated total SOD activity, which declined upon AG490 co-administration, accompanied by altered JAK phosphorylation and downstream JNK/p38/ERK signals. Conclusion: Intraperitoneal EGCG ameliorates pain and modulates PRL-JAK2‑dependent JNK/p38/ERK signaling in rat peritoneal EMs. No significant reduction in established lesion size was detected after multiple comparison correction. Further validation is needed to confirm pathway selectivity and lesion-targeted efficacy of EGCG for EMs.
Subfield: Reproductive Medicine
Field: Medicine
Domain: Health Sciences
Open Access status: green
OpenAlex ID: W7222269811
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