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Post a Comment Modeling the female hypogonadism by means of ovarian ischemization and its morphofunctional justification
- Authors: Magradze R.N.1, Lisovsky A.D.1, Lisovsky D.A.1, Popkovsky N.A.1,2, Bobkov P.S.1,2, Bayramov A.A.1, Droblenkov A.V.1,2
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Affiliations:
- Institute of Experimental Medicine
- Saint Petersburg Medico-Social Institute
- Issue: Vol 20, No 3 (2022)
- Pages: 289-295
- Section: Original study articles
- URL: https://journals.rcsi.science/RCF/article/view/112456
- DOI: https://doi.org/10.17816/RCF203289-295
- ID: 112456
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Abstract
The present study is devoted to the morphofunctional substantiation of the model of female hypogonadism, which is important for the subsequent evaluation of the effectiveness of its targeted pharmacological correction, as well as to elucidate the resistance of ovarian endocrine cells to damage as a result of experiencing a single acute ischemic effect. In three groups of adult female rats under anesthesia, the arteries of the right and left ovaries were ligated for 30, 45, and 60 min (4 rats in each group). After the operation, the wound was sutured. Sham-operated rats (4 individuals) served as controls. After 7 days, the results were analyzed. The blood levels of sex steroid hormones (17β-estradiol, progesterone) and gonadotropins (FSH and LH) were determined by enzyme-linked immunosorbent assay. In the meridional histological sections of the mature tertiary follicle and the corpus luteum of the right and left ovaries, after survey staining, the number and percentage of viable and dead endocrinocytes were counted, and the area of viable endocrine cells was determined. The significance of differences in the median, upper and lower quartiles of the compared parameters was determined using the nonparametric Mann–Whitney test. It has been established that a single acute ovarian ischemia induces massive death and degenerative changes in a significant part of the viable endocrine cells of the mature tertiary follicle and corpus luteum, most pronounced with a one-hour bilateral occlusion of the ovarian vessels. These quantitative and structural changes in interstitial endocrine cells and ovarian luteocytes cause a significant decrease in the production of sex steroids, which, in turn, causes hyperproduction of the corresponding pituitary tropins. Morphological changes in both types of ovarian endocrine cells in this model of acute single ovarian ischemia are highly sensitive; the use of a number of morphometric parameters of endocrinocytes in combination with the determination of the concentration of peripheral and regulatory homones will allow using this model to assess the effectiveness of the correction of female hypogonadism with various pharmacological preparations.
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##article.viewOnOriginalSite##About the authors
Roman N. Magradze
Institute of Experimental Medicine
Author for correspondence.
Email: droblenkov_a@mail.ru
Postgraduate Student, S.V. Anichkov Department of Neuropharmacology
Russian Federation, 12, Akademika Pavlova st., Saint Petersburg, 199376Anatoly D. Lisovsky
Institute of Experimental Medicine
Email: lisovsky.t@mail.ru
Postgraduate Student, S.V. Anichkov Department of Neuropharmacology
Russian Federation, 12, Akademika Pavlova st., Saint Petersburg, 199376Dmitry A. Lisovsky
Institute of Experimental Medicine
Email: lisovsky.t@mail.ru
Cand. Med. (Sci.), post-doc fellow, S.V. Anichkov Department of Neuropharmacology
Russian Federation, 12, Akademika Pavlova st., Saint Petersburg, 199376Nikita A. Popkovsky
Institute of Experimental Medicine; Saint Petersburg Medico-Social Institute
Email: popkovskij.nikita@yandex.ru
Postgraduate Student, S.V. Anichkov Department of Neuropharmacology
Russian Federation, 12, Akademika Pavlova st., Saint Petersburg, 199376; Saint PetersburgPavel S. Bobkov
Institute of Experimental Medicine; Saint Petersburg Medico-Social Institute
Email: bobkov_pl@mail.ru
ORCID iD: 0000-0003-4858-6170
Cand. Sci. (Med.), Senior Research Associate, S.V. Anichkov Department of Neuropharmacology
Russian Federation, 12, Akademika Pavlova st., Saint Petersburg, 199376; Saint PetersburgAlekber A. Bayramov
Institute of Experimental Medicine
Email: droblenkov_a@mail.ru
ORCID iD: 0000-0002-0673-8722
Dr. Med. Sci. (Pharmacology), Leading Research Associate, S.V. Anichkov Department of Neuropharmacology
Russian Federation, 12, Akademika Pavlova st., Saint Petersburg, 199376Andrey V. Droblenkov
Institute of Experimental Medicine; Saint Petersburg Medico-Social Institute
Email: droblenkov_a@mail.ru
ORCID iD: 0000-0001-5155-1484
Dr. Med. Sci. (Morphology), Leading Research Associate, S.V. Anichkov Department of Neuropharmacology
Russian Federation, 12, Akademika Pavlova st., Saint Petersburg, 199376; Saint PetersburgReferences
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