Aim: Endometriosis is a common, chronic benign gynecologic disease and distresses women in their reproductive age. Yet the pathogenesis of endometriosis is not clear, multifactorial mechanisms have been characterized for the initiation, progression, and regression of this disease. It has been suggested that immune cells in the lymphoid lineage play essential roles in accepting or rejecting the survival, implantation, and proliferation of endometrial and endometriotic cells and, dysfunction of B-lymphocytes (B-cells) are one of the major causes for the progression of endometriosis. In this study, we aimed to evaluate the potential therapeutic efficacy of Rituximab, an inhibitor for B-cells, for endometriosis in an experimental animal model.
Methods: Experimental endometriosis animal model has been utilized using mature female rats. Rats underwent surgery to initiate endometriosis on the abdominal wall. After confirming for endometriosis, rats were treated with either Rituximab or saline solution. After 14 days of treatment, implants were dissected, and evaluated for volumes and histological features. Anti-CD-20 antibody was used for immunohistochemistry scoring purposes.
Results: There is significant decrease in the volume of endometriotic implants after treatment with Rituximab (188.81 ± 149.42 vs 20.37 ± 13.08, p = 0.001). There are also significant differences for the B-cell count and fibrosis score between the control and treatment groups (3.08 ± 2.6 vs 1.56 ± 1.42., p = 0.043).
Conclusion: In an experimental rat endometriosis model, we assessed Rituximab, an antibody for B-lymphocyte, as a candidate medical treatment for endometriosis. Additional studies are required to further evaluate the effects of Rituximab on the prevention of endometriosis.
Keywords: B-lymphocytes; Endometriosis; Immunomodulator drugs; Rituximab.
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