Kala Manika, Nivsarkar Manish
Departments of Pharmacology and Toxicology, B.V. Patel Pharmaceutical Education and Research Development Centre, Thaltej, Ahmedabad, Gujarat 380054, India; Faculty of Pharmacy, NIRMA University, Sarkhej-Gandhinagar Highway, Gota, Ahmedabad, Gujarat 382481, India.
Departments of Pharmacology and Toxicology, B.V. Patel Pharmaceutical Education and Research Development Centre, Thaltej, Ahmedabad, Gujarat 380054, India.
Gen Comp Endocrinol. 2016 Jan 1;225:117-124. doi: 10.1016/j.ygcen.2015.09.010. Epub 2015 Sep 21.
Stress has been identified as a potential trigger for reproductive dysfunctions, but the psycho-physiological pathway behind the effect of stress on ovulation remains unexplored. The present research work highlights the plausible mechanism of psychological stress on ovulation in mice by targeting superoxide dismutase (SOD), an enzyme involved in ovulation. For this, three consecutive studies were carried out. The first study aimed to determine the effect of psychological stress induced change in cortisol level, behavioral parameters and normal estrous cyclicity. The effect on mRNA expression of SOD subtypes, follicular growth in histological sections of ovaries and the difference in oocyte quality and number, upon superovulation were assessed in the subsequent studies. The results indicate that psychological stress model causes an increase in cortisol level (p⩽0.05) with development of anhedonia, depression and anxiety. An irregular estrous cycle was observed in stressed mice with an upregulation in mRNA expression of SOD subtypes. Histological sections revealed an increase in atretic antral follicle with an impaired follicular development. Moreover, immature oocytes were obtained from superovulated stressed mice. The study concludes that psychological stress results in anovulation which may be due to increase in cortisol level and SOD activity in stressed mice.
压力已被确定为生殖功能障碍的一个潜在触发因素,但压力对排卵影响背后的心理生理途径仍未得到探索。本研究工作通过针对超氧化物歧化酶(SOD,一种参与排卵的酶),突出了心理压力对小鼠排卵的可能机制。为此,进行了三项连续的研究。第一项研究旨在确定心理压力诱导的皮质醇水平变化、行为参数和正常发情周期的影响。在随后的研究中评估了对SOD亚型mRNA表达、卵巢组织切片中卵泡生长以及超排卵时卵母细胞质量和数量差异的影响。结果表明,心理压力模型导致皮质醇水平升高(p⩽0.05),同时出现快感缺失、抑郁和焦虑。在应激小鼠中观察到发情周期不规则,SOD亚型的mRNA表达上调。组织学切片显示闭锁卵泡增加,卵泡发育受损。此外,从超排卵的应激小鼠中获得了未成熟卵母细胞。该研究得出结论,心理压力导致无排卵,这可能是由于应激小鼠中皮质醇水平和SOD活性增加所致。