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Iranian journal of nursing and midwifery research · 2026

Endometrial Expression of Angiogenesis-related Factors Following Ovarian Stimulation and Epigallocatechin Gallate Administration.

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Zamani Rarani Fahimeh, Sharifi Mohammadreza, Rashidi Bahman

Аннотация

BACKGROUND: AngiomiRs are a specialized subclass of microRNAs that target genes related to angiogenesis, such as Vascular Endothelial Growth Factor (VEGF). Angiogenesis is crucial in all stages of pregnancy and is essential for creating a receptive endometrium for embryo implantation. Both ovarian stimulation and Epigallocatechin Gallate (EGCG), a major component of green tea, can influence angiogenesis. This study aims to examine endometrial quality, with a focus on angiogenesis, as well as serum levels of estradiol and progesterone, following EGCG administration in ovarian-stimulated mice, as a valuable model for studying human reproductive health and diseases.

METHODS AND MATERIALS: Forty adult female mice were assigned to four distinct groups: 1) control, 2) ovarian stimulation (7.5 IU HMG followed by 7.5 IU HCG 48 hours later, administered intraperitoneally), 3) EGCG (5 mg/kg EGCG for 4 days, IP), and 4) ovarian stimulation + EGCG groups. Gene expression analysis of miR-16-5p was performed using real-time polymerase chain reaction. VEGF protein and CD31-positive cell density were assessed through immunohistochemistry, and serum estradiol and progesterone levels were measured using ELISA.

RESULTS: Endothelial cell density, VEGF protein, and miR-16-5p expression and estradiol concentration significantly increased in the ovarian stimulation group compared to the control group (p < 0.05). The smallest reduction in these parameters was observed in the group that received EGCG. EGCG also significantly reduced the progesterone level (p < 0.05).

CONCLUSION: EGCG significantly reduced endometrial angiogenesis, and angiomiR-16-5p may mediate the effects of EGCG on endometrial quality; however, further studies are needed.

ИП Урсолов Владлен Сергеевич

ИНН 500118482352 · ОГРНИП 314500117700049

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