Journal of Clinical Endocrinology & Metabolism , doi:10.1210/jc.2006-2486 Copyright © 2007 by The Endocrine Society Metformin Suppresses Interleukin (IL)-1ß-Induced IL-8 Production, Aromatase Activation, and Proliferation of Endometriotic Stromal CellsYuri Takemura, Yutaka Osuga, Osamu Yoshino, Akiko Hasegawa, Tetsuya Hirata, Yasushi Hirota, Emi Nose, Chieko Morimoto, Miyuki Harada, Kaori Koga, Toshiki Tajima, Tetsu Yano and Yuji TaketaniDepartment of Obstetrics and Gynecology, Faculty of Medicine, University of Tokyo, Tokyo 113-8655, Japan Address all correspondence and requests for reprints to: Yutaka Osuga, M.D., Department of Obstetrics and Gynecology, Faculty of Medicine, University of Tokyo, 7-3-1, Hongo, Bunkyo-ku, Tokyo 113-8655, Japan. E-mail: yutakaos-tky{at}umin.ac.jp. Context: Metformin, a widely used treatment for diabetes that improves insulin sensitivity, also has both antiinflammatory properties and a modulatory effect on ovarian steroid production, two actions that have been suggested to be efficacious in therapy for endometriosis. Objective: To determine whether metformin may be effective for the treatment of endometriosis, we evaluated the effects of this agent on inflammatory response, estradiol production, and proliferation of endometriotic stromal cells (ESCs). Design: ESCs derived from ovarian endometriomas were cultured with various concentrations of metformin. Main Outcome Measures: IL-8 production, mRNA expression and aromatase activity, and 5-bromo-2'-deoxyuridine incorporation in ESCs were measured. Results: Metformin dose-dependently suppressed IL-1ß-induced IL-8 production, cAMP-induced mRNA expression and aromatase activity, and 5-bromo-2'-deoxyuridine incorporation in ESCs. Conclusion: These results suggest that further investigation into the unique therapeutic potential of metformin as an antiendometriotic drug is warranted. This article has been cited by other articles:
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