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Background <p>Thin endometrium(TE) has been widely recognized as a critical factor contributing to reduced success rates of assisted reproductive technology (ART). In recent years, platelet-rich plasma (PRP) has been extensively employed in the treatment of thin endometrium; however, its underlying mechanisms remain poorly understood, and its clinical efficacy remains controversial. Given the superior therapeutic outcomes demonstrated by platelet concentrates (PCs) in regenerative medicine, the present study aimed to investigate the therapeutic potential and mechanistic basis of injectable platelet-rich fibrin (i-PRF) in an ethanol‑induced rat model of thin endometrium.</p> Methods <p>i-PRF was prepared from human blood and characterized for growth factor release and microstructure. Rats were divided into control, Model, Ethanol + NS, and Ethanol+i-PRF groups.Endometrial morphology was assessed by H&amp;E and immunohistochemistry. Receptivity was evaluated by LIF/VEGF expression and embryo implantation counts. In vitro, endometrial stromal cells (ESCs) were co-cultured with platelets, and mitochondrial transfer was tracked using MitoTracker<sup>®</sup>. Platelet mitochondrial respiration was inhibited with oligomycin/FCCP to assess functional contribution.</p> Results <p>i-PRF released VEGF-A, TGF-β1, and PDGF-AB for up to 15 days (peak at 7 days), with a dense fibrin network entrapping abundant platelets. Ethanol injection significantly reduced endometrial thickness from 409.27 ± 55.86&#xa0;μm to 104.48 ± 57.03&#xa0;μm and decreased gland number from 22.4 ± 4.34 to 9.2 ± 3.77 (both <i>p</i> &lt; 0.05).Administration of i-PRF reversed these pathological changes, restoring endometrial thickness to 464.11 ± 27.1&#xa0;μm and gland count to 29.0 ± 9.41 (*p* &lt; 0.05 vs. model). Immunohistochemical analysis revealed that i-PRF&#xa0;treatment increased the abundance of vimentin⁺,cytokeratin 18⁺ (CK-18⁺) and ki-67<sup>+</sup> cells and enhanced the expression of leukemia inhibitory factor (LIF) and vascular endothelial growth factor (VEGF). Compared with the model group, the Ethanol + i‑PRF group exhibited a markedly higher embryo number (3.88 ± 3.91, P &lt; 0.001); although this value was lower than that of the control group (5.00 ± 3.46), the difference did not reach statistical significance (P &gt; 0.05). &#xa0;In vitro co-culture of endometrial stromal cells (ESCs) with platelets promoted ESC proliferation and VEGF secretion. Confocal microscopy confirmed the direct transfer of platelet mitochondria to ESCs. Inhibition of platelet mitochondrial respiration did not block ESC proliferation but significantly suppressed VEGF and vimentin expression (<i>p</i> &lt; 0.05).</p> Conclusions <p>i-PRF effectively repairs thin endometrium in a rat model, and mitochondrial transfer from platelets to ESCs plays a key role in promoting endometrial regeneration. These findings support i-PRF as a promising therapy for TE.</p>

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Administration of injectable platelet-rich fibrin improved repair of thin endometrium via mitochondria in a rat model

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  • 发表日期：

    2026年7月23日

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  • Haiqing Tian,
  • Yixuan Zhu,
  • Haozhe Ma,
  • Nan Su,
  • Manli Zhang,
  • Xiaolin La,
  • Lei Cui,
  • Zijian Zhang,
  • Jing Dong,
  • Mengjie Zhang

摘要

Background

Thin endometrium(TE) has been widely recognized as a critical factor contributing to reduced success rates of assisted reproductive technology (ART). In recent years, platelet-rich plasma (PRP) has been extensively employed in the treatment of thin endometrium; however, its underlying mechanisms remain poorly understood, and its clinical efficacy remains controversial. Given the superior therapeutic outcomes demonstrated by platelet concentrates (PCs) in regenerative medicine, the present study aimed to investigate the therapeutic potential and mechanistic basis of injectable platelet-rich fibrin (i-PRF) in an ethanol‑induced rat model of thin endometrium.

Methods

i-PRF was prepared from human blood and characterized for growth factor release and microstructure. Rats were divided into control, Model, Ethanol + NS, and Ethanol+i-PRF groups.Endometrial morphology was assessed by H&E and immunohistochemistry. Receptivity was evaluated by LIF/VEGF expression and embryo implantation counts. In vitro, endometrial stromal cells (ESCs) were co-cultured with platelets, and mitochondrial transfer was tracked using MitoTracker®. Platelet mitochondrial respiration was inhibited with oligomycin/FCCP to assess functional contribution.

Results

i-PRF released VEGF-A, TGF-β1, and PDGF-AB for up to 15 days (peak at 7 days), with a dense fibrin network entrapping abundant platelets. Ethanol injection significantly reduced endometrial thickness from 409.27 ± 55.86 μm to 104.48 ± 57.03 μm and decreased gland number from 22.4 ± 4.34 to 9.2 ± 3.77 (both p < 0.05).Administration of i-PRF reversed these pathological changes, restoring endometrial thickness to 464.11 ± 27.1 μm and gland count to 29.0 ± 9.41 (*p* < 0.05 vs. model). Immunohistochemical analysis revealed that i-PRF treatment increased the abundance of vimentin⁺,cytokeratin 18⁺ (CK-18⁺) and ki-67+ cells and enhanced the expression of leukemia inhibitory factor (LIF) and vascular endothelial growth factor (VEGF). Compared with the model group, the Ethanol + i‑PRF group exhibited a markedly higher embryo number (3.88 ± 3.91, P < 0.001); although this value was lower than that of the control group (5.00 ± 3.46), the difference did not reach statistical significance (P > 0.05).  In vitro co-culture of endometrial stromal cells (ESCs) with platelets promoted ESC proliferation and VEGF secretion. Confocal microscopy confirmed the direct transfer of platelet mitochondria to ESCs. Inhibition of platelet mitochondrial respiration did not block ESC proliferation but significantly suppressed VEGF and vimentin expression (p < 0.05).

Conclusions

i-PRF effectively repairs thin endometrium in a rat model, and mitochondrial transfer from platelets to ESCs plays a key role in promoting endometrial regeneration. These findings support i-PRF as a promising therapy for TE.