Han Jie, Yang Danfeng, Liu Ziyi, Tian Lei, Yan Jun, Li Kang, Fang Zhen, Chen Qi, Lin Bencheng, Zhang Wei, Xi Zhuge, Liu Xiaohua
Tianjin Institute of Environmental and Operational Medicine, Tianjin 300050, China; Tianjin university of sport, Tianjin 301617, China.
Tianjin Institute of Environmental and Operational Medicine, Tianjin 300050, China.
Life Sci. 2021 Dec 1;286:120053. doi: 10.1016/j.lfs.2021.120053. Epub 2021 Oct 14.
Explore the effects of heat stress and psychological stress combined exposure on the uterus and its underlying mechanisms.
Sixty female Sprague-Dawley rats were randomly assigned to four groups: control group, psychological stress group, high ambient temperature group, and high ambient temperature combined with psychological stress group. All treatments were administered for two weeks. During this period, the estrous cycle, body weights and rectal temperature were measured regularly. Then, ovarian weight coefficient, serum estradiol (E) and progesterone (P) concentration, uterine histomorphological alterations, levels of tumor necrosis factor alpha (TNF-α), malondialdehyde (MDA) and superoxide dismutase (SOD), and the expressions of ovarian hormone receptors, leukemia inhibitory factor (LIF) and its receptor, homeobox gene A10 (HoxA10), Wnt5a, Wnt7a, β-catenin, and P-β-catenin in the uterus and endometrium were detected.
High temperature combined with psychological stress lead to body weight, body temperature, ovarian hormones and estrus cycle disorder, uterine gland ducts expansion and endometrial thickness reduction, and the decreased expression of endometrial receptivity markers (LIF and HoxA10). Further, disturbed expression of E and P receptors in endometrium, elevated MDA and TNF-α levels, and decreased Wnt5a, Wnt7a and P-β-catenin content were found. Our data suggested that co-exposure to high temperature and psychological stress could aggravate uterine damage probably by inducing ovarian hormonal disorder and the subsequent oxidative stress and inflammation, and reduce the endometrial function through suppressing Wnt signaling.
This will provide the scientific basis for improving female reproductive health, and preventing and treating reproductive disorders.
探讨热应激和心理应激联合暴露对子宫的影响及其潜在机制。
将60只雌性Sprague-Dawley大鼠随机分为四组:对照组、心理应激组、高温环境组和高温环境联合心理应激组。所有处理均持续两周。在此期间,定期测量动情周期、体重和直肠温度。然后,检测卵巢重量系数、血清雌二醇(E)和孕酮(P)浓度、子宫组织形态学改变、肿瘤坏死因子α(TNF-α)、丙二醛(MDA)和超氧化物歧化酶(SOD)水平,以及子宫和子宫内膜中卵巢激素受体、白血病抑制因子(LIF)及其受体、同源框基因A10(HoxA10)、Wnt5a、Wnt7a、β-连环蛋白和磷酸化β-连环蛋白的表达。
高温与心理应激联合导致体重、体温、卵巢激素和动情周期紊乱,子宫腺管扩张和子宫内膜厚度降低,以及子宫内膜容受性标志物(LIF和HoxA10)表达下降。此外,还发现子宫内膜中E和P受体表达紊乱,MDA和TNF-α水平升高,Wnt5a、Wnt7a和磷酸化β-连环蛋白含量降低。我们的数据表明,高温和心理应激联合暴露可能通过诱导卵巢激素紊乱以及随后的氧化应激和炎症加重子宫损伤,并通过抑制Wnt信号通路降低子宫内膜功能。
这将为改善女性生殖健康以及预防和治疗生殖障碍提供科学依据。