A MODERATE FORM OF HYPERHOMOCYSTEINEMIA IS ACCOMPANIED BY POLYPLOIDIZATION OF HEPATOCYTES

K. A. Pazinenko, N. Chuchkova, M. Smetanina
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Abstract

The aim of research is to find out the effect of hyperhomocysteinemia on the regenerative process of liver cells. The histological structure of the liver was studied in Rattus norvegicus Berk white rats (n=25) (control group - 10 animals, comparison group with moderate hyperhomocysteinemia - 15 animals). On histological sections stained with hematoxylin and eosin, the following were calculated: the number of nuclei, the proportion of binuclear cells, the area and the diameter of the nucleus; the nuclear cytoplasmic index was calculated. With the use of immunohistochemical stain by antibodies to detect the expression of the Ki-67 marker (rabbit IgG, 1:200; Cell Marque Corporation, USA), the number and intensity of expression of Ki-67-positive cells in the field of view of the microscope were determined. In the liver of animals with moderate hyperhomocysteinemia, the presence of two processes was revealed at the same time. It is reactive-dystrophic (the presence of periportal leukocyte-lymphocyte infiltrates, the appearance of cells in a state of dystrophy and necrosis) and regenerative (an increase in the core area from 52,51±4,5 to 56,68±5,58 µm, nuclear-cytoplasmic ratio, an increase in the number and intensity of Ki-67+cells expression). The presence of hepatocytes with very large nuclei (polyploid), which make up 12,5 % of the entire population is characteristic of homocysteine-induced liver pathology. Hyperhomocysteinemia, along with a decrease in the number and dystrophy of individual hepatocytes, leads to an increase in the diameter and area of the cell nucleus, an increase in the intensity of proliferation, the appearance of polyploid nuclei, which increases the regenerative potential of the liver and provides a crucial role in the homeostasis of the gland. The findings require further research to determine the "critical point" of transition, which will allow modulation of liver tissue function.
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中度高同型半胱氨酸血症伴肝细胞多倍体化
本研究旨在探讨高同型半胱氨酸血症对肝细胞再生过程的影响。研究褐家鼠Berk大鼠肝脏组织结构(n=25)(对照组10只,中度高同型半胱氨酸血症对照组15只)。在苏木精和伊红染色的组织学切片上,计算细胞核的数量、双核细胞的比例、细胞核的面积和直径;计算核细胞质指数。采用免疫组化抗体染色法检测Ki-67标记物(兔IgG, 1:20 00;Cell Marque Corporation, USA),测定显微镜视野内ki -67阳性细胞的表达数量和表达强度。在中度高同型半胱氨酸血症动物的肝脏中,同时存在两个过程。它是反应性营养不良(门静脉周围存在白细胞淋巴细胞浸润,细胞呈营养不良和坏死状态)和再生(核心区从52,51±4,5增加到56,68±5,58µm,核质比,Ki-67+细胞表达的数量和强度增加)。大核肝细胞(多倍体)的存在,占整个人群的12.5%,是同型半胱氨酸诱导的肝脏病理的特征。高同型半胱氨酸血症,伴随着单个肝细胞数量的减少和营养不良,导致细胞核直径和面积的增加,增殖强度的增加,多倍体核的出现,这增加了肝脏的再生潜力,并在腺体的稳态中起着至关重要的作用。这一发现需要进一步的研究来确定过渡的“临界点”,这将允许肝脏组织功能的调节。
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