Vitamin A accelerates the process of liver regeneration in the initial stages of Сu - induced fibrosis

Anatoly Bozhkov, Svitlana Bilovetska
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 Materials and methods: Experiments were conducted on 20 sexually mature male Wistar rats, which were divided into 4 groups: a control group that was not exposed to copper sulfate and vitamin A, a group that was at the initial stage of liver fibrosis, which was provided by three consecutive administrations of copper sulfate at a dose of 1 mg/100 g of weight (one series of injections), a group that was at the stage of intensive development of fibrosis (F2), which was carried out by two consecutive series of copper sulfate injections with an interval of 3 days between injections, and a group that received vitamin A three times daily in a dose of 300 IU/100 g of weight between two series of intoxication. Body weight dynamics, relative liver weight, histological changes in liver tissues and the number of binuclear hepatocytes were determined.
 Results: It has been found that animals with Cu-induced liver fibrosis did not gain or lose body weight, and the introduction of vitamin A ensured the restoration of body weight growth, and they slightly lagged behind the control group. In animals with liver fibrosis that received vitamin A, the relative weight of the liver was slightly increased and there were 2 times more binuclear hepatocytes. The structural organization of the liver tissue changed to a minor extent, and to the greatest extent there was an increase in the thickness of the Glisson’s capsule, in which immunocompetent cells were incorporated.
 Conclusions: Vitamin A contributed to the normalization of liver function against the background of the development of fibrosis. The mechanism of normalization can be ensured due to an increase in the number of binuclear hepatocytes, a slight increase in the relative weight of the liver, and was accompanied by an increase in the thickness of the Glisson’s capsule, in which immunocompetent cells were incorporated","PeriodicalId":21636,"journal":{"name":"ScienceRise: Biological Science","volume":"38 1","pages":"0"},"PeriodicalIF":0.0000,"publicationDate":"2023-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"ScienceRise: Biological Science","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.15587/2519-8025.2023.288227","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
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Abstract

Aim: To test the hypothesis about the possible role of vitamin A in normalizing the functional activity of the liver with Cu-induced fibrosis by increasing the regeneration process. Materials and methods: Experiments were conducted on 20 sexually mature male Wistar rats, which were divided into 4 groups: a control group that was not exposed to copper sulfate and vitamin A, a group that was at the initial stage of liver fibrosis, which was provided by three consecutive administrations of copper sulfate at a dose of 1 mg/100 g of weight (one series of injections), a group that was at the stage of intensive development of fibrosis (F2), which was carried out by two consecutive series of copper sulfate injections with an interval of 3 days between injections, and a group that received vitamin A three times daily in a dose of 300 IU/100 g of weight between two series of intoxication. Body weight dynamics, relative liver weight, histological changes in liver tissues and the number of binuclear hepatocytes were determined. Results: It has been found that animals with Cu-induced liver fibrosis did not gain or lose body weight, and the introduction of vitamin A ensured the restoration of body weight growth, and they slightly lagged behind the control group. In animals with liver fibrosis that received vitamin A, the relative weight of the liver was slightly increased and there were 2 times more binuclear hepatocytes. The structural organization of the liver tissue changed to a minor extent, and to the greatest extent there was an increase in the thickness of the Glisson’s capsule, in which immunocompetent cells were incorporated. Conclusions: Vitamin A contributed to the normalization of liver function against the background of the development of fibrosis. The mechanism of normalization can be ensured due to an increase in the number of binuclear hepatocytes, a slight increase in the relative weight of the liver, and was accompanied by an increase in the thickness of the Glisson’s capsule, in which immunocompetent cells were incorporated
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维生素A在Сu诱导的纤维化的初始阶段加速肝脏再生的过程
目的:验证维生素A可能通过促进肝再生过程而促进铜诱导肝纤维化肝脏功能活动正常化的假说。材料与方法:实验选用20只性成熟雄性Wistar大鼠,分为4组:对照组,没有接触到硫酸铜和维生素a,一群在肝纤维化的最初阶段,这是连续三个政府提供的硫酸铜的剂量1毫克/ 100克的重量(注射系列之一),一组是集约发展阶段的纤维化(F2),这是由两个连续的一系列的硫酸铜注射注射之间的间隔3天,另一组在两次中毒期间每天服用三次维生素a,剂量为300国际单位/100克体重。测定大鼠体重动态、相对肝脏重量、肝脏组织组织学变化及双核肝细胞数量。 结果:已发现铜诱导肝纤维化动物的体重不增不减,维生素A的引入保证了体重增长的恢复,且与对照组相比略有滞后。肝纤维化动物服用维生素A后,肝脏的相对重量略有增加,双核肝细胞增加2倍。肝组织的结构组织发生轻微改变,最大程度上是Glisson 's包膜厚度增加,包膜中加入了免疫活性细胞。 结论:在纤维化发生的背景下,维生素A有助于肝功能的正常化。双核肝细胞数量增加,肝脏相对重量略有增加,并伴有Glisson 's包膜厚度增加,其中纳入了免疫活性细胞,从而保证了正常化的机制
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