卵巢缺血对女性性腺功能减退的模拟及其形态功能论证

R.N. Magradze, Anatoly D. Lisovsky, Dmitry A. Lisovsky, N. A. Popkovsky, P. S. Bobkov, A. A. Bayramov, A. Droblenkov
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引用次数: 0

摘要

本研究致力于女性性腺功能减退模型的形态功能证实,这对于后续评估其靶向药物纠正的有效性,以及阐明卵巢内分泌细胞对单一急性缺血效应造成的损伤的抵抗具有重要意义。三组成年雌性大鼠麻醉后,分别结扎左右卵巢动脉30min、45min和60min(每组4只)。手术后,缝合了伤口。假手术大鼠(4只)作为对照。7天后,对结果进行分析。采用酶联免疫吸附法测定血清性类固醇激素(17-雌二醇、孕酮)和促性腺激素(FSH、LH)水平。在左右卵巢成熟第三卵泡和黄体经经组织学切片上,经调查染色,计数活的和死的内分泌细胞数量和百分比,并测定活的内分泌细胞面积。比较参数的中位数、上、下四分位数差异的显著性采用非参数曼惠特尼检验。已经证实,卵巢单次急性缺血可导致大量成熟第三卵泡和黄体的存活内分泌细胞大量死亡和退行性改变,最明显的是卵巢血管阻塞1小时。间质内分泌细胞和卵巢黄体细胞的这些数量和结构变化导致性类固醇的产生显著减少,而性类固醇的产生又导致相应的垂体促激素的过量产生。急性单卵巢缺血模型中两类卵巢内分泌细胞形态学变化高度敏感;使用一些内分泌细胞的形态测量参数,结合外周激素和调节激素浓度的测定,将允许使用该模型来评估各种药物制剂纠正女性性腺功能减退的有效性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Modeling the female hypogonadism by means of ovarian ischemization and its morphofunctional justification
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 (17-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 MannWhitney 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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