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

Alfi Ruham Burjiah
Ashon Sa’adi
Widjiati Widjiati


Background: Endometriosis is a common, benign, estrogen-dependent, and chronic gynecological disease. Immune system disturbance 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.

Aim: This research aimed to study the effect of different doses of vitamin D on Interleukin-17 (IL-17) expression in endometriosis mice models.

Methods: Endometriosis was induced in 24 mice divided into 4 groups of 6. Group C received no treatment, while groups T1, T2, and T3 received graded doses of oral vitamin D, sequentially 8, 16, and 24 IU, for 3 weeks. IL-17 expression and the extent of endometriotic peritoneal lesions were then  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.

Results: Endometriosis lesions decreased after 16 and 24 IU of vitamin D administration (p 0.023 and 0.009). Endometriosis lesion also tends to be  smaller after 8 IU of vitamin D supplementation, although insignificant (p > 0.05). IL-17 expression was significantly lower after 24 IU vitamin D  administration compared to the untreated group (p = 0.004). Lower IL-17 expressions were also observed after 8 and 16 IU vitamin D administration,  although insignificant (p = 0.452 and p = 0.645). 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 IL-17 in endometriotic lesions, vitamin D inhibited the development  endometriotic lesions in the  endometriosis mice model. The recommended vitamin D dose in this study was 24 IU. 

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eISSN: 2218-6050
print ISSN: 2226-4485