Vitamin D inhibited endometriosis development in mice model through interleukin 17 modulation

Abstract

Background: Endometriosis is a common benign, estrogen-dependent, and chronic gynecological disease. Immune system disturbances and inflammatory abnormalities were involved in the pathogenesis of endometriosis. , Therefore, it is logical to use vitamin D, which has an immunomodulatory capacity, as supportive therapy for endometriosis. Aims: This research time to study the effect of different doses of vitamin D on IL-17 expression in endometriosis mice models. Methods: Endometriosis was induced in twenty-four mice divided into four groups of six. Group C received no treatment, while groups T1, T2, and T3 received graded doses of vitamin D to the stomach, sequentially 8 IU, 16 IU, and 24 IU for three weeks. Interleukin-17 expression and the extent of endometriotic peritoneal lesions were also measured and analyzed. Statistical tests were performed to see the difference in the mean area of endometriosis lesions and IL-17 expression between the control and treatment groups, as well as the correlation between the extent of endometriosis lesions and IL-17. We performed a statistical test to determine whether stratified doses have different IL-17 and endometriosis area outcomes. Results: The area of endometriosis lesions was decreased after 16 IU and 24 IU of vitamin D administration (p 0.023 and 0.009). Endometriosis lesions also tended to be smaller after 8 IU of vitamin D supplementation, although insignificant (p > 0.05). Interleukin-17 expression was significantly lower after 24 IU vitamin D administration (p = 0.004). Vitamin D doses of 8 IU and 16 IU caused lower IL-17 expression, although not significant (p = 0.452 and p = 0.645). The regulation of IL-17 expression was significantly dependent on the dose level of vitamin D with an optimal dose of 24 IU (p = 0.004). This dose also caused the smallest endometriosis lesion, although not optimal (p > 0.05). IL-17 expression was moderately and positively correlated with the extent of endometriosis lesions (p = 0.012, rho = 0.505). Conclusion: By modulating the expression of interleukin-17 in endometriotic lesions, vitamin D inhibits the development of endometriotic lesions in the endometriosis mice model. The optimal vitamin D dose in this study was 24 IU.