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Objective: To determine the effects of oxytocin (OT) on surgically induced endometriosis in a rat model., Study Design: Twelve female Sprague-Dawley rats were included. After the implantation and establishment of autologous endometrium onto the abdominal wall peritoneum, the rats were randomly divided into two groups, treated with intramuscular oxytocin (OT group, 160μgkg/day, n=6) or isotonic NaCl solution (control group, 1mLkg/day, n=6) for 28 days. To evaluate the therapeutic effects of OT, the explant volumes were calculated and the levels of vascular endothelial growth factor (VEGF), monocyte chemotactic protein-1, and TNF-α were measured in plasma and peritoneal fluid. Endometriotic explants were examined histologically by semiquantitative analysis., Results: After treatment, the mean endometriotic explant volume was decreased in the OT group (p=0.016). The histopathological score and VEGF immunoexpression of endometriotic explants were significantly lower in the OT group (p=0.007) than in controls (p=0.000). Inflammatory cytokine levels in plasma and peritoneal fluid were considerably decreased in the OT group. Moreover, TUNEL immunohistochemistry clearly demonstrated more apoptotic changes in the mononuclear cells of the OT group compared with controls., Conclusion: We suggest that oxytocin might be considered as a potential candidate therapeutic agent for endometriosis., (Copyright © 2014 Elsevier Ireland Ltd. All rights reserved.)

The main aim of this study is to describe the in vivo temporal and spatial expression of monocyte chemotactic protein 1 (MCP-1) in human endometrial endothelial cells (HEECs) and to compare the in vitro regulation of MCP-1 expression by sex steroids in HEECs from women with or without endometriosis. Eutopic endometrial tissues and endometriosis implants were grouped according to the menstrual cycle phase and were examined by immunohistochemistry for MCP-1 expression. No significant difference was observed for MCP-1 immunoreactivity in the endothelial cells of eutopic endometrium of women with endometriosis when compared to endometrium of women without endometriosis and to endometriosis implants. For in vitro studies, the purity of cultured HEECs (90%-95%) was confirmed by immunocytochemistry using endothelium-specific markers CD31 and CD146. The effects of estradiol (5 x 10(- 8) mol/L), progesterone (10(-7) mol/L), or both on MCP-1 messenger RNA (mRNA) and protein levels were analyzed by reverse transcriptase-polymerase chain reaction (RT-PCR) analysis and enzyme-linked immunosorbent serologic assay (ELISA), respectively. Sex steroids did not have significant effect on MCP-1 mRNA and protein expression in HEECs from women without endometriosis. However, we observed that the sex steroid treatment stimulated MCP-1 mRNA and protein expression in HEECs from women with endometriosis (P < .05). We postulate that the stimulation of chemokine expression by sex steroids in the endometrial endothelial cells in women with endometriosis may play a central role in recruiting mononuclear cells, therefore contributing to the inflammatory aspect of endometriosis.

Objective: To investigate the expression and localization of interleukin-8 (IL-8) and monocyte chemotactic protein 1 (MCP-1) in women with and without endometriosis., Design: Comparative immunohistochemical study., Setting: Academic medical center., Patient(s): Ectopic (n = 24) and homologous eutopic endometrium (n = 24) from women with endometriosis and endometrium from women without endometriosis (n = 27) were used for immunohistochemical analysis of IL-8 and MCP-1., Intervention(s): Tissue sections were immunostained with antihuman IL-8 and MCP-1 antibodies., Main Outcome Measure(s): Microscopic evaluation to assess the presence and localization of IL-8 and MCP-1 throughout the menstrual cycle in both eutopic endometrial and endometriotic tissues of women with endometriosis and comparison with normal endometrium., Result(s): In normal endometrium, secretory phase samples expressed higher levels of epithelial IL-8 than in proliferative phase samples. Epithelial MCP-1 expression was similar in both proliferative and secretory phases. Proliferative phase samples showed higher epithelial IL-8 and MCP-1 expressions in eutopic endometrium of women with endometriosis compared with that of normal women. Immunoreactivities of both chemokines were significantly increased in the epithelial cells of ectopic endometrial tissues compared with those of normal endometrium., Conclusion(s): These findings suggest that IL-8 and MCP-1 may be involved in the pathogenesis of endometriosis.

Background: To clarify the inflammatory nature of adenomyosis, we aimed to investigate the expression of interleukin-8 (IL-8) and monocyte chemotactic protein-1 (MCP-1) by immunohistochemistry to determine their putative role in pathophysiology of adenomyosis., Methods: Adenomyosis samples, with their eutopic endometrium, were collected from 30 women undergoing hysterectomy. Endometrium from 27 women without adenomyosis were also collected as a control group. Samples were grouped according to the menstrual cycle phase and examined by immunohistochemistry for IL-8 and MCP-1., Results: In normal endometrium, secretory phase samples expressed higher levels of epithelial IL-8 than in proliferative phase samples (P = 0.01), and we observed a trend for an increased epithelial MCP-1 expression in the secretory phase samples compared with the proliferative phase samples (P = 0.07). Endometrial samples of women with adenomyosis did not show the same cyclic variation. In the secretory phase, eutopic endometrium of women with adenomyosis expressed lower levels of epithelial IL-8 and MCP-1 compared with normal endometrium (P < 0.05). The expression of epithelial IL-8 and MCP-1 was higher in the adenomyosis foci than the eutopic endometrium (P < 0.05)., Conclusions: These findings may indicate that an intrinsic abnormality of inflammatory response may be present in eutopic endometrium of women with adenomyosis, and IL-8 and MCP-1 may contribute to the pathophysiology of adenomyosis.