Melatonin Alleviates Perimenopausal Sleep Disorders by Regulating the Expression of MTNR1A and Hormone Level: A Retrospective Study

Abstract

Background: Sleep disorder, frequently observed among perimenopausal women, decreases quality of life. Melatonin is reported to ameliorate circadian imbalances and thus can be employed as a treatment for perimenopausal sleep disorder patients. We attempted to clarify whether and how melatonin affects perimenopausal sleep disorders. Methods: Study patients consisted of 120 perimenopausal women divided into 3 groups: (i) perimenopausal women without sleep disorder (n = 60); (ii) those with sleep disorder but without melatonin treatment (n = 30); and (iii) those with sleep disorder with melatonin treatment (n = 30). During the period March 2019 to December 2019, the following data was collected and analyzed: Pittsburgh Sleep Quality index (PSQI) score, sex hormones, melatonin, melatonin 1A receptor (MTNR1A), protein kinase A (PKA), extracellular signal-regulated kinase 1/2 (ERK1/2), phosphorylation-PKA (p-PKA), and p-ERK1/2 levels. We compared these data between the groups. Results: Melatonin administration showed the following in female patients with postmenopausal sleep disorder: (1) significantly decreased the PSQI scores, (2) up-regulated melatonin levels and MTNR1A protein expression, (3) promoted the phosphorylation pathway of the PKA-ERK1/2 pathway in peripheral blood, and (4) significantly improved follicle-stimulating hormone (FSH), luteinizing hormone (LH) and estradiol (E2) levels. Melatonin administration had no significant effect on progesterone (P), testosterone (T) or prolactin (PRL). Conclusions: Melatonin therapy alleviated perimenopausal sleep disorders. Up-regulation of MTNR1A expression and improvement of the hormone balance were also observed, which may the reason for the observed sleep-disorder-amelioration. Melatonin has the potential to be a useful option for perimenopausal sleep disorders.

Borolatonin limits cognitive deficit and neuron loss while increasing proBDNF in ovariectomised rats

“…Hence, the role of borolatonin as an antioxidant or as a melatonin receptor agonist and its selectivity should be evaluated by means of binding assays. Additionally, this could be suggested by utilizing antagonists of the melatonin receptors on steroid deprivation due to the diversity of the effects of melatonin (and probably borolatonin) in steroid-depleted animals or humans [72][73][74]. In addition, the exploration of alternative mechanisms of action should be evaluated as compounds with a similar chemical structure that exert action on serotonin receptors [69], on ionic channels, or on the expression of the BDNF [69].…”