El-Malkey Nanees Fouad, Aref Mohammed, Emam Hassan, Khalil Sama Salah
Physiology Department, Faculty of Medicine, Zagazig University, Al Sharqiya, Egypt.
Anatomy and Embryology Department, Faculty of Veterinary Medicine, Zagazig University, Al Sharqiya, Egypt.
Reprod Sci. 2021 Aug;28(8):2278-2291. doi: 10.1007/s43032-021-00497-3. Epub 2021 Feb 16.
Preeclampsia (PE) is a leading cause of stroke and cognitive impairment in the offspring. Melatonin is involved in the outcome of normal pregnancy. Its receptors are widespread in the embryo. This study aimed to investigate the fetal neuroprotective effect of melatonin in experimentally induced PE. After induction of pregnancy in 18 female rats, they were divided into three equal groups. PE was induced in groups II and III by injection of deoxycorticosterone acetate and drinking isotonic saline. Melatonin was supplied to group III orally (10 mg/kg body weight) throughout pregnancy. Pregnancy was terminated on day 20, and macroanatomical investigation of three fetuses from each pregnant rat and their placentae was performed. Placental and brain homogenates were analyzed for malondialdehyde (MDA), placental growth factor (PLGF), tumor necrosis factor-α (TNF-α), and brain transforming growth factor-β (TGF-β). Histopathological analysis of fetal brain sections was performed. Melatonin improved placental, fetal, and brain weight; significantly reduced fetal death rate; significantly increased PLGF, placental and brain superoxide dismutase, and brain TGF-β; and significantly decreased placental TNF-α and brain MDA. Brain micromorphological study found normal glial cells and neuropil in the melatonin-treated group and a loss of neuronal cell outlines with an accumulation of cellular debris in the untreated group. In conclusion, melatonin approximately showed a neuroprotective activity by managing PE-induced oxidative stress in the placenta and fetal cerebral cortex of rats.
子痫前期（PE）是后代中风和认知障碍的主要原因。褪黑素参与正常妊娠的结局。其受体在胚胎中广泛分布。本研究旨在探讨褪黑素在实验性诱导的PE中对胎儿的神经保护作用。18只雌性大鼠怀孕后，被分为三组，每组数量相等。通过注射醋酸脱氧皮质酮和饮用等渗盐水，在第二组和第三组诱导PE。在整个孕期，第三组大鼠口服褪黑素（10mg/kg体重）。在第20天终止妊娠，并对每只怀孕大鼠的三个胎儿及其胎盘进行大体解剖学研究。分析胎盘和脑匀浆中的丙二醛（MDA）、胎盘生长因子（PLGF）、肿瘤坏死因子-α（TNF-α）和脑转化生长因子-β（TGF-β）。对胎儿脑切片进行组织病理学分析。褪黑素改善了胎盘、胎儿和脑的重量；显著降低了胎儿死亡率；显著增加了PLGF、胎盘和脑超氧化物歧化酶以及脑TGF-β；并显著降低了胎盘TNF-α和脑MDA。脑微观形态学研究发现，褪黑素治疗组的神经胶质细胞和神经纤维正常，而未治疗组的神经元细胞轮廓消失，细胞碎片堆积。总之，褪黑素通过控制大鼠胎盘和胎儿大脑皮质中PE诱导的氧化应激，大致显示出神经保护活性。
