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Abstract：
Severe preeclampsia is one of the most serious obstetric diseases. However, the pathogenesis of the disease is not fully understood. In the present study, placental artery and blood serum was collected from patients with severe preeclampsia, as well as from normal pregnant women. The results of reverse transcription-quantitative (q)PCR, western blotting, and immunohistochemical staining revealed markedly decreased transient receptor potential cation channel subfamily V member 1 (TRPV1), ATP-sensitive potassium channel (KATP) subtype Kir6.1/SUR2B and endothelial nitric oxide synthase (eNOS) expression in severe preeclampsia tissue specimens compared with those in samples from normal pregnant women. The nitrate reduction method indicated lower NO levels in the tissue specimens and serum of patients with severe preeclampsia. Moreover, hematoxylin-eosin staining showed that the endothelial cell layer in the placental artery of patients with severe preeclampsia was notably damaged. To investigate the potential role of TRPV1-KATP channels in severe preeclampsia, HUVECs were used for in vitro experiments. The samples were divided into a control group, a TRPV1 agonist group (capsaicin) and a TRPV1 inhibitor group (capsazepine). qPCR and western blotting revealed that the relative gene and protein expression levels of TRPV1, Kir6.1, SUR2B and eNOS in the control group were significantly lower than those in the capsaicin group and considerably higher than those in the capsazepine group. Based on previous studies and the results of the present study, we hypothesized that impairment of the endothelial TRPV1-KATP channels results in decreased eNOS/NO pathway activity, which may be one of the mechanisms involved in severe preeclampsia. The increase in NO generation mediated by TRPV1-KATP may be a suitable target for the management of severe preeclampsia.
摘要：
重度子痫前期是最严重的产科疾病之一。然而,该病的发病机制尚不完全清楚。在本研究中,从重度子痫前期患者收集胎盘动脉和血清，以及正常孕妇。逆转录定量（q）PCR的结果，西方印迹,免疫组织化学染色显示瞬时受体电位阳离子通道亚家族V成员1（TRPV1）显著降低，与正常孕妇的样本相比，重度子痫前期组织标本中ATP敏感性钾通道（KATP）亚型Kir6.1/SUR2B和内皮型一氧化氮合酶（eNOS）的表达。硝酸盐还原法表明重度子痫前期患者的组织标本和血清中NO水平较低。此外，苏木精-伊红染色显示重度子痫前期患者胎盘动脉内皮细胞层明显受损。探讨TRPV1-KATP通道在重度子痫前期中的潜在作用。HUVEC用于体外实验。将样本分为对照组，TRPV1激动剂组(辣椒素)和TRPV1抑制剂组(辣椒素)。qPCR和蛋白质印迹显示，对照组TRPV1，Kir6.1，SUR2B和eNOS的相对基因和蛋白质表达水平显着低于辣椒素组，而明显高于辣椒素组。根据以往的研究和本研究的结果，我们假设内皮TRPV1-KATP通道受损导致eNOS/NO通路活性降低，这可能是重度子痫前期的发病机制之一。TRPV1-KATP介导的NO产生的增加可能是治疗重度先兆子痫的合适目标。
