Impact of chronic incomplete sleep deprivation on ovarian reserve function in mice
Objective To explore the effect of chronic incomplete sleep deprivation(SD)on ovarian reserve function in mice and its potential mechanisms.Methods Sixteen 7-8 week old female C57BL/6 SPF mice were randomly divided into control and SD groups(n=8 per group)after one week of acclimatization.The mice in the SD group were treated with SD from 7:00 to 10:00 using a deprivation rod for a total of 40 d.Before the first day and the last day of the experiment,vaginal smears were collected daily for 9 d to record and evaluate the estrous cycle.On the last day of the experiment,serum levels of estradiol,progesterone,follicle-stimulating hormone(FSH),luteinizing hormone(LH),and melatonin(MT)were measured by enzyme-linked immunosorbent assay(ELISA).The ovaries were dissected to calculate the ovarian index and count the number of primordial follicles by hematoxylin-eosin(HE)staining.Cardiac perfusion was performed to get the brains and the expression of c-Fos protein was observed in the suprachiasmatic nucleus(SCN)by immunohistochemistry.Results Compared with control group,SD group had a tendency of estrous cycle disorders.Hormone levels of estradiol[(20.19±3.67)ng/L],progesterone[(2.88±0.53)μg/L],and FSH[(13.42±2.36)U/L]in the SD group were significantly lower than those in control group[(24.66±2.15)ng/L,P=0.010;(3.43±0.49)μg/L,P=0.049;(17.01±1.49)U/L,P=0.003].Hormone levels of LH and MT in the SD group were lower than those in control group,but without statistical significances(all P＞0.05).There was no significant change in the number of primordial follicles between the two groups(P＞0.05).However,the oocyte morphology was poor,the granulosa cells were disorderedly arranged,the number of atretic follicles was decreased,and ovarian fibrosis was obvious in the SD group.Immunohistochemical staining showed an upregulation of c-Fos protein expression in the SCN of the SD group.Conclusion Continuous 3 h SD for 40 d impairs ovarian reserve function in mice,possibly related to excessive activation of the SCN.
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