Liu Guanhui, Dong Yulan, Wang Zixu, Cao Jing, Chen Yaoxing
Laboratory of Veterinary Anatomy, College of Animal Medicine, China Agricultural University , Beijing , China.
Stress. 2014 Dec;17(6):494-503. doi: 10.3109/10253890.2014.966263.
The influence of stress on embryo implantation is not well understood. Prior studies have focused on later gestational stages and the long-term impact of stress on immune function. The objective of this study is to investigate the effects of restraint stress on the immune parameters and the oxidative states of the uterus during implantation. In this study, pregnant CD1 mice were subjected to restraint stress (4 h/d) on embryonic day 1 (E1) and sacrificed on E3, E5, and E7. Maternal plasma corticosterone (CORT) secretion and implantation sites in the uterus were examined. The uterine (excluding embryos) homogenate and uterine lymphocytes were collected to examine oxidative stress states and associated immune parameters. The results demonstrated that restraint stress increased maternal plasma CORT secretion and reduced the number of implantation sites by 15.3% on E5 and by 26.1% on E7. Moreover, restraint stress decreased the density of uterine natural killer (uNK) cells in the endometrium by 22.1-47.9% and increased the density of mast cells in the myometrium by 55.6-76.9%. Restraint stress remarkably decreased the CD3(+)CD4(+) T/CD3(+)CD8(+) T cell ratio (by 26.2-28.9%) and attenuated uterine lymphocyte proliferation and secretion of cytokines. In addition, restraint stress threatened the intracellular equilibrium between oxidants and antioxidants, resulting in decreased glutathione peroxidase (GSH-PX) (32.2% and 45.7%), superoxide dismutase (SOD) (15.5% and 26.1%), and total antioxidant capacity (T-AOC) (18.4% and 18.2%) activities and increased malondialdehyde (MDA) (34.4% and 43.0%) contents on E5 and E7. In conclusion, these findings demonstrate that restraint stress causes abnormal implantation and negatively impacts immune parameters in association with oxidative stress in mice.
应激对胚胎着床的影响尚未完全明确。先前的研究主要集中在妊娠后期以及应激对免疫功能的长期影响。本研究的目的是探讨束缚应激对着床期间子宫免疫参数和氧化状态的影响。在本研究中，妊娠CD1小鼠在胚胎第1天（E1）接受束缚应激（4小时/天），并于E3、E5和E7处死。检测母体血浆皮质酮（CORT）分泌及子宫着床部位。收集子宫（不包括胚胎）匀浆和子宫淋巴细胞，检测氧化应激状态及相关免疫参数。结果表明，束缚应激增加了母体血浆CORT分泌，E5时着床部位数量减少了15.3%，E7时减少了26.1%。此外，束缚应激使子宫内膜中子宫自然杀伤（uNK）细胞密度降低了22.1%-47.9%，使子宫肌层中肥大细胞密度增加了55.6%-76.9%。束缚应激显著降低了CD3(+)CD4(+)T/CD3(+)CD8(+)T细胞比值（降低了26.2%-28.9%），并减弱了子宫淋巴细胞增殖和细胞因子分泌。此外，束缚应激破坏了细胞内氧化剂和抗氧化剂之间的平衡，导致E5和E7时谷胱甘肽过氧化物酶（GSH-PX）活性降低（分别降低32.2%和45.7%）、超氧化物歧化酶（SOD）活性降低（分别降低15.5%和26.1%）以及总抗氧化能力（T-AOC）活性降低（分别降低18.4%和18.2%），同时丙二醛（MDA）含量增加（分别增加34.4%和43.0%）。总之，这些研究结果表明，束缚应激会导致小鼠着床异常，并对与氧化应激相关的免疫参数产生负面影响。
