Kocal Emel, Atilgan Remzi, Pala Şehmus, Aslan Melike, Kuloğlu Tuncay, Ilhan Nevin, Önalan Ebru Etem, Hançer Serhat, Bircan Gizem Kaymaz
Department of Obstetrics and Gynecology, Firat University School of Medicine, Elazig, Turkey.
Department of Histology and Embriology, Firat University School of Medicine, Elazig, Turkey.
Reprod Sci. 2025 Jun 18. doi: 10.1007/s43032-025-01913-8.
Ovarian hyperstimulation syndrome (OHSS) is a life-threatening complication that usually develops as a result of triggering ovulation with human chorionic gonadotropin (hCG) after gonadotropin treatment, and in whose pathophysiology vascular endothelial growth factor (VEGF) and inflammatory mediators play a role. Nifedipine, used especially in the treatment of hypertension, is a calcium channel blocker. Nifedipine also has anti-inflammatory effects via transient receptor potential canonical (TRPC1) ion channel inhibition. VEGF also regulates the angiogenic process through TRPC channels. In our study, we investigated the potential of nifedipine to prevent OHSS due to its TRPC1 blocking effect and anti-inflammatory effects. A total of 28 rats were randomly divided into four equal groups. Group (G) 1 control group (n = 7). Rats in G2 (n = 7) were administered 30 IU pregnant mare serum gonadotropin for 4 days and OHSS was induced by administering 30 IU hCG on the fifth day. Rats in G3 (n = 7) were induced to have OHSS and were given 100 μg/kg oral cabergoline, while rats in G4 (n = 7) were induced to have OHSS and were given 20 mg/kg intraperitoneal nifedipine. On the fifth day, all rats were decapitated and VEGF, interleukin (IL)-1β, IL-6, tumor necrosis factor (TNF)-α, and hypoxia-inducible factor (HIF)-1α levels were measured in their serum and tissues. TRPC1 gene expression and immunohistochemical analysis were performed in ovarian tissue. We showed that nifedipine inhibited VEGF and some inflammatory factor levels more than cabergoline. We showed that nifedipine may achieve these effects through TRPC1 blockade and suppression of inflammatory factors.
卵巢过度刺激综合征（OHSS）是一种危及生命的并发症，通常在促性腺激素治疗后用人绒毛膜促性腺激素（hCG）触发排卵时发生，血管内皮生长因子（VEGF）和炎症介质在其病理生理过程中起作用。硝苯地平，尤其用于治疗高血压，是一种钙通道阻滞剂。硝苯地平还通过抑制瞬时受体电位经典型（TRPC1）离子通道发挥抗炎作用。VEGF也通过TRPC通道调节血管生成过程。在我们的研究中，我们研究了硝苯地平因其TRPC1阻断作用和抗炎作用预防OHSS的潜力。总共28只大鼠被随机分为四组，每组7只。第1组为对照组（n = 7）。第2组（n = 7）的大鼠连续4天给予30 IU孕马血清促性腺激素，并在第5天给予30 IU hCG诱导OHSS。第3组（n = 7）的大鼠诱导产生OHSS并给予100 μg/kg口服卡麦角林，而第4组（n = 7）的大鼠诱导产生OHSS并给予20 mg/kg腹腔注射硝苯地平。在第5天，所有大鼠断头处死，检测其血清和组织中VEGF、白细胞介素（IL）-1β、IL-6、肿瘤坏死因子（TNF）-α和缺氧诱导因子（HIF）-1α的水平。在卵巢组织中进行TRPC1基因表达和免疫组化分析。我们发现硝苯地平比卡麦角林更能抑制VEGF和一些炎症因子水平。我们发现硝苯地平可能通过TRPC1阻断和抑制炎症因子来实现这些作用。
