Pedrycz Agnieszka, Siermontowski Piotr
Department of Histology and Embryology medical University in Lublin, Poland.
Department of Maritime and Hyperbaric Medicine Military Institute of Medicine, Gdynia, Poland.
Ann Agric Environ Med. 2017 Mar 31;24(1):121-128. doi: 10.5604/12321966.1230677.
Kidney damage during pregnancy constitutes a diagnostic and therapeutic challenge. However, it is not entirely known whether a kidney condition recognised before the pregnancy releases an organism's response to pregnancy, or whether pregnancy itself worsens kidney function.
The aim of the study was immunohistochemical evaluation of cells of kidneys of pregnant rats under the influence of nitric oxide (NO), with measurement of the immunoexpression of cellular stress markers (p-53, HSP 70). The dose of administered L-arginine (NO substrate) was approximated to that applied in obstetrics in gestosis prevention and treatment in pregnant women.
60 female rats used in experiment were divided into 6 groups: 3 experimental and 3 control. The females from experimental groups were administered L-arginine (40g/kg, per os) every other day starting from the seventh day or pregnancy. The animals were decapitated on the 10th, 20th day of pregnancy, and 10 days after the delivery. Kidneys taken from decapitated rats were evaluated using the immunohistochemical three step method. HSP 70 and p-53 proteins were detected.
L-arginine increased the expression of p-53 protein - on the 10th day of pregnancy, which increased at the end of pregnancy; however, 10 days after delivery the level dropped below that observable during physiological pregnancy. Hormonal changes in physiological pregnancy cause an increase in expression of the p-53 (cell stress marker) in the epithelial cells of renal tubules, mainly at the end of pregnancy (20th day). 10 days after the delivery, this expression decreases. The expression of HSP-70 protein increases already on the 10th day of pregnancy and maintains a similar level throughout the pregnancy, but is reduced after the puerperium.
孕期肾脏损伤构成了诊断和治疗方面的挑战。然而，目前尚不完全清楚妊娠前已确诊的肾脏疾病是否会引发机体对妊娠的反应，或者妊娠本身是否会使肾功能恶化。
本研究旨在通过免疫组化评估一氧化氮（NO）作用下妊娠大鼠肾脏细胞，并测量细胞应激标志物（p-53、热休克蛋白70，HSP 70）的免疫表达。所给予的L-精氨酸（NO底物）剂量近似于产科用于预防和治疗孕妇妊娠中毒症时的用药剂量。
实验使用的60只雌性大鼠分为6组：3个实验组和3个对照组。从妊娠第7天开始，实验组的雌性大鼠每隔一天经口给予L-精氨酸（40g/kg）。在妊娠第10天、第20天以及分娩后10天对动物实施断头处死。采用免疫组化三步法对断头处死大鼠的肾脏进行评估。检测HSP 70和p-53蛋白。
L-精氨酸使p-53蛋白的表达增加——在妊娠第10天增加，在妊娠末期进一步升高；然而，分娩后10天该水平降至生理妊娠期间可观察到的水平以下。生理妊娠期间的激素变化导致肾小管上皮细胞中p-53（细胞应激标志物）的表达增加，主要在妊娠末期（第20天）。分娩后10天，这种表达下降。HSP-70蛋白的表达在妊娠第10天就已增加，并在整个妊娠期间维持在相似水平，但在产褥期后降低。
