Although advances in the prediction and management of ovarian hyperstimulation syndrome (OHSS) have been introduced, complete prevention is not yet possible. Previously, we and other authors have shown that vascular endothelial growth factor, angiopoietins (ANGPTs) and sphingosine-1-phosphate are involved in OHSS etiology. In addition, we have demonstrated that ovarian protein levels of platelet-derived growth factor (PDGF) ligands -B and -D decrease in an OHSS rat model, whilst PDGFR-β and ANGPT2 remain unchanged. In the present work, we investigated the role of PDGF-B in OHSS by evaluating ligand protein levels in follicular fluid (FF) from women at risk of developing OHSS and by using an immature rat model of OHSS. We demonstrated that PDGF-B and PDGF-D are lower in FF from women at risk of developing OHSS compared to control patients (P < 0.05). In the OHSS rat model, PDGF-B (0.5 µg/ovary) administration decreased ovarian weight (P < 0.05), reduced serum progesterone (P < 0.05) and lowered the percentage of cysts (P < 0.05), compared to untreated OHSS rats, but had no effect on the proportion of follicles or corpora lutea (CL). PDGF-B treatment also restored the expression of steroidogenic acute regulatory protein (P < 0.05) and P450 cholesterol side-chain cleavage enzyme (P < 0.01) to control levels. In addition, PDGF-B increased the peri-endothelial cell area in CL and cystic structures, and reduced vascular permeability compared to untreated OHSS ovaries. Lastly, PDGF-B increased the levels of junction proteins claudin-5 (P < 0.05), occludin (P < 0.05) and β-catenin (P < 0.05), while boosting the extracellular deposition of collagen IV surrounding the ovarian vasculature (PP < 0.01), compared to OHSS alone. In conclusion, our findings indicate that PDGF-B could be another crucial mediator in the onset and development of OHSS, which may lead to the development of novel prediction markers and therapeutic strategies.

中文翻译：

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血小板衍生生长因子 B 恢复血管屏障完整性并降低卵巢过度刺激综合征的通透性。

尽管在卵巢过度刺激综合征 (OHSS) 的预测和管理方面取得了进展，但还不可能完全预防。以前，我们和其他作者已经表明血管内皮生长因子、血管生成素 (ANGPT) 和 1-磷酸鞘氨醇与 O​​HSS 病因有关。此外，我们已经证明，在 OHSS 大鼠模型中，血小板衍生生长因子 (PDGF) 配体 -B 和 -D 的卵巢蛋白水平降低，而 PDGFR-β 和 ANGPT2 保持不变。在目前的工作中，我们通过评估有患 OHSS 风险的女性的卵泡液 (FF) 中的配体蛋白水平并使用未成熟的 OHSS 大鼠模型来研究 PDGF-B 在 OHSS 中的作用。我们证明，与对照患者相比，有发生 OHSS 风险的女性的 FF 中的 PDGF-B 和 PDGF-D 较低。P  < 0.05)。在 OHSS 大鼠模型中 ，与未治疗的 OHSS 大鼠相比，PDGF-B（0.5 µg/卵巢）给药可降低卵巢重量（P  < 0.05），降低血清孕酮（P  < 0.05）并降低囊肿百分比（P < 0.05） ，但对卵泡或黄体 (CL) 的比例没有影响。PDGF-B 治疗还使类固醇生成急性调节蛋白 ( P  < 0.05) 和 P450 胆固醇侧链裂解酶 ( P  < 0.01)的表达恢复到对照水平。此外，与未处理的 OHSS 卵巢相比，PDGF-B 增加了 CL 和囊状结构中的内皮细胞面积，并降低了血管通透性。最后，PDGF-B 增加了连接蛋白 claudin-5 的水平（P  < 0.05)、occludin ( P  < 0.05) 和 β-catenin ( P  < 0.05)，同时 与单独的 OHSS 相比，促进卵巢脉管系统周围胶原蛋白 IV 的细胞外沉积 ( PP < 0.01)。总之，我们的研究结果表明，PDGF-B 可能是 OHSS 发生和发展的另一个关键介质，这可能会导致新的预测标志物和治疗策略的发展。