Melatonin improves endometrial receptivity of adenomyosis mice via the NF-κB signaling pathway

Abstract

Background: Adenomyosis is a benign gynecological disorder but has detrimental effect on female fertility of childbearing age. Melatonin is a classic antioxidant and free radical scavenger to protect against tissue damage, and exerts important roles in reproductive systems. The effects of melatonin on endometrial development in adenomyosis remain unclear. This study aimed to explore the function of melatonin on endometrial development in adenomyosis mice and its possible mechanisms. Methods: Inducing an adenomyosis mouse model by oral administration of tamoxifen. 0, 10, 20, 30, 50 mg/kg body weight melatonin were then respectively injected to investigate the effect of melatonin on implantation rates. Quantitative real time polymerase chain reaction (qRT-PCR), western blotting and immunohistochemistry were used to determine the expression of endometrial receptivity markers in endometrium during implantation window. Endometrial mRNA expressions of implantation-associated，oxidative stress-correlated and apoptosis-related genes were analyzed by qRT-PCR. Western blotting was used to explore the mechanism of protective effect of melatonin on endometrial development. Results: 30mg/kg melatonin injection significantly improved the number of implantation sites in an adenomyosis model mice. Adenomyosis adversely effected the development of mouse uterine development and impaired endometrial receptivity. Melatonin administration ameliorated hyper-inflammation state of the endometrium, improved antioxidant capacity and depressed apoptosis of endometrial cells induced by adenomyosis to reduce reproductive damage by suppressing the NF-κB signaling pathway. Conclusion: Melatonin treatment ameliorates impaired endometrial development and endometrial receptivity of adenomyosis mice by improving the microenvironment of endometrium via NF-κB signaling pathway. The current study suggests the potential efficacy of melatonin based adenomyosis therapy.