Epigallocatechin Gallate and Prolactin JAK2 Related Signaling in Experimental Endometriosis An Integrated Analysis of In Vivo and In Vitro Models

Xi Ye, Xuanxuan Hong, Runzhi Shi, Wenxin Ha, Yangyang Tan, 孙宁, Yi Wei, Ruxue Zhou, Le Yu, Liehong Wang
2026 · doi:10.5281/zenodo.23357771 · W7222269811
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Intraperitoneal epigallocatechin gallate alleviates pain and modulates prolactin-JAK2 signaling in rat peritoneal endometriosis, though it does not significantly reduce established lesion volumes.

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This study evaluated the therapeutic potential of intraperitoneal epigallocatechin gallate (EGCG) in a rat model of autologous peritoneal endometriosis. The researchers found that EGCG significantly alleviated pain behaviors and reduced proinflammatory cytokines, while transcriptomic analysis indicated modulation of the prolactin-JAK2-mediated JNK/p38/ERK signaling cascade. However, despite increasing antioxidant activity, the treatment did not result in a statistically significant reduction in established lesion volume after correcting for multiple comparisons. This paper is centrally about endometriosis — specifically investigating the molecular mechanisms and symptomatic relief provided by EGCG in an experimental rat model of the disease.

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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.
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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.

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