Hamza Reham Z, Diab Abdel Aziz A, Zahra Mansour H, Asalah Ali K, Moursi Suzan M M, Al-Baqami Najah M, Al-Salmi Fawziah A, Attia Mai S
Biology Department, Faculty of Sciences, Taif University, P.O. Box 11099, Taif 21944, Saudi Arabia.
Zoology Department, Faculty of Science, Zagazig University, Zagazig 44519, Egypt.
Int J Endocrinol. 2021 Nov 15;2021:5017362. doi: 10.1155/2021/5017362. eCollection 2021.
Preeclampsia (PE) is one of the commonest causes for maternal and fetal morbidity and mortality. Imbalances of angiogenic factors, oxidative stress, and inflammatory response have a role in the pathogenesis of PE. Data regarding the circulating apelin level and its role in PE remains controversial. This study was formulated to assess the serum apelin level in PE, investigate its correlation with some inflammatory, oxidative stress, and angiogenic proteins in a nitric oxide synthase inhibitor; the N (gamma)-nitro-L-arginine methyl ester (L-NAME)-induced rat model of PE and determine whether apelin administration could protect against development of PE. 40 healthy adult female albino rats and 10 adult male albino rats were used in this study. The pregnant female rats were randomly divided into three groups: group 1 (normal pregnant group), group 2 (PE-induced group), injected subcutaneously with 75 mg L-NAME/kg bodyweight/day starting from day 9 to 20 of gestation, and group 3 (PE-induced group supplemented with apelin (PE + apelin)); PE induced as before and simultaneously subcutaneously injected with apelin-13 (6 × 10 mol/kg bodyweight/twice daily) beginning from day 6 to 20 of gestation. In all groups, blood pressure and urine protein were determined at gestation days (GD) 0, 10, and 18. Moreover, serum apelin, placental growth factor (PLGF), vascular endothelial growth factor (VEGF), soluble fms-like tyrosine kinase-1 (sFlt-1), soluble endoglin (sEng), interferon-gamma (IFN-), and interleukin-10 (IL-10) levels and serum superoxide dismutase enzyme (SOD) and catalase (CAT) activities of all groups were estimated at the end of experiment. Placental histopathological examination was also performed. PE-induced rats showed significantly decreased serum apelin levels. Moreover, they showed significantly increased blood pressures, urine proteins, sFlt-1, sEng, and IFN- (mean arterial blood pressure, urine proteins, sFlt-1, sEng, and IFN- showed significant negative correlations with serum apelin level), but it showed significantly decreased VEGF, PLGF, IL-10, SOD, and CAT (VEGF, PLGF, IL-10, and SOD showed significant positive correlations with serum apelin level). In contrast, exogenous apelin administration significantly ameliorated these parameters together with improvement in the placental histoarchitecture in the apelin-supplemented PE group. This study demonstrated the protective effects of apelin administration on the pathogenesis of PE.
子痫前期（PE）是孕产妇和胎儿发病及死亡的最常见原因之一。血管生成因子失衡、氧化应激和炎症反应在PE的发病机制中起作用。关于循环中Apelin水平及其在PE中的作用的数据仍存在争议。本研究旨在评估PE患者血清Apelin水平，研究其与一氧化氮合酶抑制剂中一些炎症、氧化应激和血管生成蛋白的相关性；用N（γ）-硝基-L-精氨酸甲酯（L-NAME）诱导的大鼠PE模型，并确定给予Apelin是否可以预防PE的发生。本研究使用了40只健康成年雌性白化大鼠和10只成年雄性白化大鼠。将怀孕的雌性大鼠随机分为三组：第1组（正常怀孕组），第2组（PE诱导组），从妊娠第9天至20天皮下注射75mg L-NAME/kg体重/天，第3组（补充Apelin的PE诱导组（PE+Apelin））；如前所述诱导PE，并从妊娠第6天至20天同时皮下注射Apelin-13（6×10mol/kg体重/每日两次）。在所有组中，在妊娠第0、10和18天测定血压和尿蛋白。此外，在实验结束时评估所有组的血清Apelin、胎盘生长因子（PLGF）、血管内皮生长因子（VEGF）、可溶性fms样酪氨酸激酶-1（sFlt-1）、可溶性内皮糖蛋白（sEng）、干扰素-γ（IFN-）和白细胞介素-10（IL-10）水平以及血清超氧化物歧化酶（SOD）和过氧化氢酶（CAT）活性。还进行了胎盘组织病理学检查。PE诱导的大鼠血清Apelin水平显著降低。此外，它们的血压、尿蛋白、sFlt-1、sEng和IFN-显著升高（平均动脉血压、尿蛋白、sFlt-1、sEng和IFN-与血清Apelin水平呈显著负相关），但VEGF、PLGF、IL-10、SOD和CAT显著降低（VEGF、PLGF、IL-10和SOD与血清Apelin水平呈显著正相关）。相比之下，外源性给予Apelin可显著改善这些参数，并改善补充Apelin的PE组的胎盘组织结构。本研究证明了给予Apelin对PE发病机制的保护作用。
