Dehydroepiandrosterone induces ovarian and uterine hyperfibrosis in female rats
Abstract
STUDY QUESTION: Do dehydroepiandrosterone (DHEA)-treated rats with polycystic ovary syndrome (PCOS) demonstrate a high level of fibrosis in ovarian and uterine tissues?
SUMMARY ANSWER: DHEA induces ovarian and uterine hyperfibrosis in rats, probably involving a transforming growth factor-β (TGF-β)-dependent mechanism.
WHAT IS KNOWN ALREADY: Chronic inflammation is the typical cause of fibrosis and is involved in the pathophysiological process of PCOS. Patients with PCOS are reported to have a higher serum level of TGF-β, a well-characterized key pro-fibrotic factor. Fibrillin-3, a protein capable of interacting with TGF-β, has been reported to be partially responsible for the fetal origin of PCOS.
STUDY DESIGN, SIZE, DURATION: Female Sprague-Dawley rats were treated with a vehicle control or DHEA for 35 days, with subsequent analyses of changes in morphology and gene expression in ovarian and uterine tissues. Rescue groups treated with metformin or simvastatin and their corresponding controls were also analyzed. A total of 80 rats were included.
PARTICIPANTS/MATERIALS, SETTING, METHODS: The PCOS model was induced by daily administration of DHEA s.c. to 3-week-old female rats, and the rescue groups were injected daily with either metformin or simvastatin in addition to DHEA. Serum steroid hormone levels were measured by enzyme-linked immunosorbent assay. Samples were stained with hematoxylin and eosin for histological morphology, and Sirius Red and immunohistochemistry for…
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