Niknafs Behrooz, Shokrzadeh Naser, Reza Alivand Mohammad, Bakhtiar Hesam Shariati Mohammad
Immunology Research Center, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran.
Infertility and Reproductive Health Research Center, Health Research Institute, Babol University of Medical Sciences, Babol, Iran.
Int J Reprod Biomed. 2022 Feb 18;20(1):47-58. doi: 10.18502/ijrm.v20i1.10408. eCollection 2022 Jan.
The role of glucocorticoids in implantation has been demonstrated.
This study aimed to evaluate the effect of dexamethasone on endometrial receptivity.
In this experimental study, 40 BALB/c female mice aged eight wk old weighing approximately 25.0 1.4 gr were used. The mice were divided into four groups (n = 10/each) of control, dexamethasone (100 μg/kg, intraperitoneal injection), mammalian target of rapamycin (mTOR) inhibitor (PP242) (30 mg/kg, intraperitoneal injection), and dexamethasone and PP242. The endometrial epithelium of the mouse was separated to measure messenger RNA expression of heart and neural crest derivatives-expressed protein 2 (), Msh homeobox 1 (), heparin binding epidermal growth factor (), microRNA (miRNA) Let-7a, miRNA-145 and miRNA-451, using real-time polymerase chain reaction. Also, protein expression of mammalian mTOR and eukaryotic translation initiation factor 4E-binding protein1 (4E-BP1) was measured using western blot.
The results revealed that the expression of , , , miRNA-451, and miRNA-Let-7a was significantly decreased in the endometrium in the dexamethasone group compared to the control, while the expression of miRNA-145 in the endometrium was up-regulated. Additionally, the administration of PP242, known as an inhibitor of mTOR, was associated with significantly reduced expression of , , , miRNA-451, and miRNA-Let-7a, while PP242 induced messenger RNA expression of miRNA-145.
It appears that dexamethasone can diminish uterine receptivity during the implantation period, at least to some extent, through the alteration of particular genes that impact endometrial receptivity. Furthermore, the mTOR pathway seemingly showed an essential role in endometrial receptivity.
糖皮质激素在着床过程中的作用已得到证实。
本研究旨在评估地塞米松对子宫内膜容受性的影响。
在本实验研究中，使用了40只8周龄、体重约25.0±1.4克的BALB/c雌性小鼠。将小鼠分为四组（每组n = 10）：对照组、地塞米松组（100μg/kg，腹腔注射）、雷帕霉素靶蛋白（mTOR）抑制剂（PP242）组（30mg/kg，腹腔注射）以及地塞米松与PP242联合组。分离小鼠子宫内膜上皮，采用实时聚合酶链反应测量心脏和神经嵴衍生表达蛋白2（）、Msh同源盒1（）、肝素结合表皮生长因子（）、微小RNA（miRNA）Let-7a、miRNA-145和miRNA-451的信使核糖核酸表达。此外，采用蛋白质印迹法测量哺乳动物mTOR和真核翻译起始因子4E结合蛋白1（4E-BP1）的蛋白质表达。
结果显示，与对照组相比，地塞米松组子宫内膜中、、、miRNA-451和miRNA-Let-7a的表达显著降低，而子宫内膜中miRNA-145的表达上调。此外，作为mTOR抑制剂的PP242给药与、、、miRNA-451和miRNA-Let-7a的表达显著降低相关，而PP242诱导miRNA-145信使核糖核酸表达。
似乎地塞米松可在着床期至少在一定程度上通过改变影响子宫内膜容受性的特定基因来降低子宫容受性。此外，mTOR通路似乎在子宫内膜容受性中发挥重要作用。
