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Objective The aim of the present study was to analyze the expression of the CD63, S100A6, and GNB2L1genes, which participate in mechanisms related to the complex pathophysiology of endometriosis. Methods A case-control study was conducted with 40 women who were diagnosed with endometriosis, and 15 fertile and healthy women. Paired samples of eutopic endometrium and endometriotic lesions (peritoneal and ovarian endometriotic implants) were obtained from the women with endometriosis in the proliferative (n = 20) or secretory phases (n = 20) of the menstrual cycle. As controls, paired endometrial biopsy samples were collected from the healthy women in the proliferative (n = 15) and secretory (n = 15) phases of the same menstrual cycle. We analyzed the expression levels of the CD63, S100A6, and GNB2L1 genes by real-time polymerase chain reaction. Results An increase in CD63, S100A6, and GNB2L1 gene transcript levels was observed in the ectopic implants compared with the eutopic endometrium of the women with and without endometriosis, regardless of the phase of the menstrual cycle. Conclusion These findings suggest that the CD63, S100A6, and GNB2L1 genes may be involved in the pathogenesis of endometriosis, since they participate in mechanisms such as inhibition of apoptosis, angiogenesis and cell proliferation, which lead to the loss of cell homeostasis in the ectopic endometrium, thus contributing to the implantation and survival of the tissue in the extrauterine environment.

Endometriosis is characterized by the growth of endometrial tissue outside the uterine cavity. The prevalence of endometriosis among women experiencing pain, infertility, or both is as high as 35% to 50%. The most common symptoms of endometriosis are dysmenorrhea, dyspareunia, chronic pelvic pain, and infertility. Evidence has suggested that endometriosis symptoms result from a local inflammatory peritoneal reaction caused by ectopic endometrial implants that undergo cyclic bleeding. On the other hand, regular physical exercise seems to have protective effects against diseases that involve inflammatory processes such as type 2 diabetes and colon and breast cancer. On this basis, it is possible that the practice of physical exercise may have beneficial effects on endometriosis. Therefore, the objective of this study was to evaluate the possible anti-inflammatory effect of physical exercise on endometriosis experimentally induced in rats. Seventy female Wistar rats were divided into 7groups of 10 animals each. Animals performed light exercise (swimming once a week), moderate exercise (swimming 3 times a week), and intense exercise (swimming 5 times a week) before or after endometriosis induction. At the end of the experimental protocol, a reduction in the size of endometriotic lesions was observed after physical exercise regardless of its frequency, with a greater reduction in the groups practicing moderate and intense activity; an increase in FAS levels and a decrease in matrix metalloproteinases 9 and proliferating cell nuclear antigen (PCNA)levels was also observed. The immunohistochemistry results did not lead to conclusive results. As expected, oxidative stress was reduced in all groups. These results show that the practice of physical exercise could be beneficial, at least in part, for the treatment of endometriosis.