An improved method for experimental modeling of premature ovarian insufficiency in Wistar rats

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Abstract

BACKGROUND: Despite an enormous progress in the field of reproductive endocrinology, the mechanisms of premature ovarian insufficiency have not been fully understood so far. Knowledge of the supposed causes and mechanisms underlying the development of premature ovarian insufficiency has expanded significantly in recent years, mainly due to advances in genetics and the creation of models for experimental research. The experimental modeling of premature ovarian insufficiency, which is as close as possible to the origin and development of the corresponding disease in humans, is effectively used to elaborate promising therapeutic approaches, in particular, to test new drugs or biologically active agents in order to study their preventive or curative effects. This article discusses the main methods of the experimental modeling of POI in laboratory animals. We have herein summarized the literature data related to the development of the clinical and morphological picture of the disease, with the advantages and disadvantages of each of the models analyzed.

AIM: The aim of this study was to modify the premature ovarian insufficiency modeling methodology to substantiate the effectiveness and to test new directions in drug therapy with subsequent implementation in clinical practice.

MATERIALS AND METHODS: The new method is based on the creation of an experimental premature ovarian insufficiency model in female Wistar rats. To obtain this model, experimental rats were randomized into two groups: 1) animals receiving cyclophosphamide at a dose of 150 mg/kg b.w. subcutaneously once (n = 10); 2) animals receiving 2 ml of saline intraperitoneally once (n = 9). On day10, the animals were removed from the experiment. After autopsy, a visual assessment of morphological changes in the ovaries was carried out, and a right-sided ovariectomy was performed.

RESULTS: When using the proposed model, the reproducibility rate of POI has reached 100%.

CONCLUSIONS: Our modification of the method ensures the creation of a highly reproducible premature ovarian insufficiency model in Wistar rats. Another significant advantage of this modeling method is its ease of implementation and economic efficiency.

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About the authors

Karina A. Zakurayeva

The Research Institute of Obstetrics, Gynecology and Reproductology named after D.O. Ott

Author for correspondence.
Email: zakuraevak@icloud.com
ORCID iD: 0000-0002-8128-306X
SPIN-code: 5215-7869
Russian Federation, Saint Petersburg

Maria I. Yarmolinskaya

The Research Institute of Obstetrics, Gynecology and Reproductology named after D.O. Ott

Email: m.yarmolinskaya@gmail.com
ORCID iD: 0000-0002-6551-4147
SPIN-code: 3686-3605

MD, Dr. Sci. (Med.), Professor of the Russian Academy of Sciences

Russian Federation, Saint Petersburg

Nikita A. Adamenkov

Oryol Regional Clinical Hospital; Turgenev Oryol State University

Email: nikita-ad@mail.ru
ORCID iD: 0000-0002-0238-2941
SPIN-code: 3348-8250
Russian Federation, Oryol; Oryol

Elena V. Potapova

Turgenev Oryol State University

Email: potapova_ev_ogu@mail.ru
ORCID iD: 0000-0002-9227-6308
SPIN-code: 9315-8770

Cand. Sci. (Tech.), Assistant Professor

Russian Federation, Oryol

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Supplementary files

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2. Fig. 1. Rat ovary after induction of premature ovarian insufficiency: complete absence of follicles. Hematoxylin and eosin staining, zoom ×100

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3. Fig. 2. Rat ovary after induction of premature ovarian insufficiency: unchanged ovarian tissue from a control rat. Hematoxylin and eosin staining, zoom ×100

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