Abstract

Endometrial receptivity is a physiological state in which the endometrium obtains an adhesive phenotype that allows embryo implantation and have a role in the problem of implantation failure. Endometrial receptivity disorders can be caused by interference with the Hypothalamus-Pituitary-Gonad (HPG) axis due to the activation of the Hypothalamus-Pituitary-Adrenal (HPA) axis by stress. HB-EGF is a biomarker of endometrial receptivity that plays a role in the decidualization of endometrial stromal cells to reach the receptive state and initiation of implantation. Corticosterone is the dominant glucocorticoid hormone in rodents, as is cortisol in humans. High corticosterone due to chronic stress triggers disruption of homeostasis in the endometrium by resulting in decreased levels of HB-EGF. This study aims to find out the effect of increased corticosterone levels due to chronic stress on HB-EGF expression in endometrium Rattus norvegicus. This research has obtained ethical eligibility from the Research Ethics Commission of the Faculty of Medicine Airlangga University. The samples on this study were 34 rat (Rattus norvegicus) which were divided into 2 groups, the control group and the stress treatment group using the Chronic Unpredictable Mild Stress (CUMS) method. Corticosterone level were obtain from blood serum detected via ELISA and HB EGF expression was obtained from endometrial in diestrus phase was evaluated by immunohistochemical methods. Corticosterone levels in the stress treatment group were higher (72.84 ± 64.03) than in the control group (23.29 ± 8.42). HB-EGF expression in the stress treatment group was lower (82.06 ± 5.91) than in the control group (118.76 ± 13.20). Statistical tests showed significant differences in HB-EGF expression in endometrium Rattus norvegicus p = 0,000 (p <0.05). Elevated level of corticosterone can decrease HB-EGF expression in endometrium Rattus norvegicus.

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