Background: Endometriosis, which is the appearance of endometrial tissue outside the uterus, is a chronic, inflammatory and estrogen-dependent disease characterized by the growth of endometrial tissue outside the uterine cavity. Immune system responses, nutrition, exercise and etc are among the most important factors affecting this disease. The aim of the present study was to evaluation of TLR4-myD88 pathway after a period of exercise in endometriosis rat.

Materials and Methods: 25 female Wistar rats were selected and divided into 5 different groups. After induction of endometriosis, exercise mice swam 5 days a week. The vitamin E group took the supplement as a gavage at a dose of 200 mg per kilogram of body weight daily. 24 hours after the end of the study, the mice were blood sampled and after killing the transplanted tissues related to endometriosis areas, they were evaluated for histological and genetic studies. The proteins studied in the present study included TLR4 and MyD88. In order to test the research hypotheses, one-way analysis of variance and Bonferroni post hoc test were used and a significance level of P≤0.05 was considered.

Results: The results showed that there was a significant difference between the research groups. The results of Bonferroni post hoc test showed that the expression level of MyD88 gene in healthy control group differed from endometriosis model control groups (P=0.0001), exercise group (P=0.019) and patient control group+vitamin E supplement (P=0.021). Significantly, the control group of endometriosis model was significantly different from the exercise group (P=0.002), the patient control group + vitamin E supplement (P=0.002) and the patient group+vitamin E+exercise (P=0.0001). There was a significant difference in the expression of TLR4 gene in the healthy control group with the control group of endometriosis model (P=0.048).

Conclusion: These results showed that induction of endometriosis strongly affects this pathway to cause inflammation in the tissue. Exercise with enzymatic adaptations may help slow the pathway and prevent inflammation and tissue cell proliferation.