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This version published online on May 15, 2007
Journal of Clinical Endocrinology & Metabolism, doi:10.1210/jc.2006-2486
A more recent version of this article appeared on August 1, 2007
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Right arrow Female Endocrinology

Submitted on November 13, 2006
Accepted on May 7, 2007

Metformin suppresses IL-1{beta}-induced IL-8 production, aromatase activation and proliferation of endometriotic stromal cells

Yuri 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 Taketani

Department of Obstetrics and Gynecology, Faculty of Medicine, University of Tokyo, Tokyo, Japan

* To whom correspondence should be addressed. E-mail: yutakaos-tky{at}umin.ac.jp.

Context: Metformin, a widely used treatment for diabetes that improves insulin sensitivity, also has both anti-inflammatory 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 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 BrdU incorporation in ESCs were measured.

Results: Metformin dose-dependently suppressed IL-1{beta}-induced IL-8 production, cAMP-induced mRNA expression and aromatase activity, and BrdU incorporation in ESCs.

Conclusions: These results suggest that further investigation into the unique therapeutic potential of metformin as an anti-endometriotic drug is warranted.
Key words: metformin • endometriosis • interleukin-8 • aromatase • proliferation




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