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<article article-type="research-article" dtd-version="1.3" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xml:lang="ru"><front><journal-meta><journal-id journal-id-type="publisher-id">actabiomedica</journal-id><journal-title-group><journal-title xml:lang="ru">Acta Biomedica Scientifica</journal-title><trans-title-group xml:lang="en"><trans-title>Acta Biomedica Scientifica</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">2541-9420</issn><issn pub-type="epub">2587-9596</issn><publisher><publisher-name>Scientific Centre for Family Health and Human Reproduction Problems</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.29413/ABS.2024-9.3.23</article-id><article-id custom-type="elpub" pub-id-type="custom">actabiomedica-4835</article-id><article-categories><subj-group subj-group-type="heading"><subject>Research Article</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="ru"><subject>ЭКСПЕРИМЕНТАЛЬНЫЕ ИССЛЕДОВАНИЯ</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>EXPERIMENTAL RESEARCHES</subject></subj-group></article-categories><title-group><article-title>Биохимические и гистологические изменения на двух моделях неалкогольной жировой болезни печени различной степени тяжести</article-title><trans-title-group xml:lang="en"><trans-title>Biochemical and histological changes in two nonalcoholic fatty liver disease models of different severity</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0001-7468-8563</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Брус</surname><given-names>Т. В.</given-names></name><name name-style="western" xml:lang="en"><surname>Brus</surname><given-names>T. V.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Брус Татьяна Викторовна – кандидат медицинских наук, доцент кафедры патологической физиологии с курсом иммунопатологии</p><p>194100, г. Санкт-Петербург, ул. Литовская, 2</p></bio><bio xml:lang="en"><p>Tatiana V. Brus – Cand. Sc. (Med.), Associate Professor at the Department of Pathological Physiology with the Course of Immunopathology</p><p>Litovskaya str. 2, Saint Petersburg 194100</p></bio><email xlink:type="simple">bant.90@mail.ru</email><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-8539-7128</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Васильев</surname><given-names>А. Г.</given-names></name><name name-style="western" xml:lang="en"><surname>Vasiliev</surname><given-names>A. G.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Васильев Андрей Глебович – д.м.н., профессор, заведующий кафедрой патологической физиологии с кусом иммунопатологии</p><p>194100, г. Санкт-Петербург, ул. Литовская, 2</p></bio><bio xml:lang="en"><p>Andrei G. Vasiliev – Dr. Sc. (Med.), Professor, Head of the Department of Pathological Physiology with the course of Immunopathology</p><p>Litovskaya str. 2, Saint Petersburg 194100</p></bio><email xlink:type="simple">avas7@mail.ru</email><xref ref-type="aff" rid="aff-1"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru"><institution>ФГБОУ ВО «Санкт-Петербургский государственный педиатрический медицинский университет» Минздрава&#13;
России</institution></aff><aff xml:lang="en"><institution>St. Petersburg State Pediatric Medical University</institution></aff></aff-alternatives><pub-date pub-type="collection"><year>2024</year></pub-date><pub-date pub-type="epub"><day>24</day><month>07</month><year>2024</year></pub-date><volume>9</volume><issue>3</issue><fpage>230</fpage><lpage>238</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Брус Т.В., Васильев А.Г., 2024</copyright-statement><copyright-year>2024</copyright-year><copyright-holder xml:lang="ru">Брус Т.В., Васильев А.Г.</copyright-holder><copyright-holder xml:lang="en">Brus T.V., Vasiliev A.G.</copyright-holder><license xml:lang="ru" license-type="creative-commons-attribution" xlink:href="https://creativecommons.org/licenses/by/4.0/" xlink:type="simple"><license-p>Данная работа распространяется под лицензией Creative Commons Attribution 4.0.</license-p></license><license xml:lang="en" license-type="creative-commons-attribution" xlink:href="https://creativecommons.org/licenses/by/4.0/" xlink:type="simple"><license-p>This work is licensed under a Creative Commons Attribution 4.0 License.</license-p></license></permissions><self-uri xlink:href="https://www.actabiomedica.ru/jour/article/view/4835">https://www.actabiomedica.ru/jour/article/view/4835</self-uri><abstract><p>Введение. Одним из приоритетных исследований современной медицины, объединяющих интересы различных специалистов (терапевтов, кардиологов, гастроэнтерологов, эндокринологов), является изучение патогенеза и заболеваний неалкогольной жировой болезни печени (НАЖБП), для которой характерна распространённость и безусловная инновационность. Поиск адекватных экспериментальных моделей НАЖБП, отражающих степень тяжести повреждения печени, имеет первостепенное значение для изучения её этиологии и патогенеза.Цель исследования. Определение биохимических маркеров для определения степени тяжести неалкогольной жировой болезни печени.Материалы и методы. В эксперименте использовались два варианта модели НАЖБП: лёгкий – неалкогольный стеатоз (НАС), тяжёлый – неалкогольный стеатогепатит (НАСГ). Измеряли следующие биохимические показатели: активность ферментов аланинаминотрансферазы (АЛТ), аспартатаминотрансферазы (АСТ), лактатдегидрогеназы (ЛДГ), щелочной фосфатазы (ЩФ), глюкозы в плазме, общего белка (ОБ), общего билирубина (ОБил) и его прямых соединений (ПБ), состояния в плазме гомоцистеина, холестерина (ОХ), триацилглицеридов (ТГ), каталазы (Кат), супероксиддисмутазы (СОД) и малонового диальдегида (МДА).Результаты. На моделях стеатогепатита функция печени нарушается в значительно большей степени, чем при стеатозе; этот фактор проявился в динамике повышения АЛТ, АСТ, ЩФ, ОХ, ОБил, МДА (p &lt; 0,001) и снижения Кат, СОД (p &lt; 0,05), что способствует развитию более выраженных проявлений пигментного и липидного обмена, цитолитических и холестатических синдромов, активации ПОЛ и депрессии антиоксидантной системы при моделировании неалкогольного стеатогепатита. Также выявлена различная степень выраженности морфологических изменений в экспериментальных группах.Выводы. Исследование показало приоритетность определения биохимических маркеров, в том числе уровней АЛТ, АСТ, ОБил, ТГ, МДА и СОД, для оптимизации лабораторной методики диагностики степени тяжести дистрофии печени.Практическая оригинальность результатов заключается в оптимизации методологии лабораторной диагностики степени тяжести патологического процесса при НАЖБП.</p></abstract><trans-abstract xml:lang="en"><p>Background. One of the priority areas of modern medicine, which unites the interests of various specialists (therapists, cardiologists, gastroenterologists, endocrinologists), is the study of the pathogenesis and clinical manifestations of nonalcoholic fatty liver disease (NAFLD), which is widespread and of unconditional social significance. The search for adequate experimental models of NAFLD that reflect the severity of liver damage is of paramount importance for studying its etiology and pathogenesis.The aim of the study. To compare biochemical and histological changes in experimental models of NAFLD of varying severity.Materials and methods. Two NAFLD model versions were used: a light one – nonalcoholic steatosis (NAS) and a severe variant – non-alcoholic steatohepatitis (NASH). The following biochemical parameters were measured: enzyme activity of alanine aminotransferase (ALT), aspartate aminotransferase (AST), lactate dehydrogenase (LDH), alkaline phosphatase (AP), plasma glucose concentration, total protein (TP), total bilirubin (TBil) and its conjugate fraction (CB), plasma concentrations of homocysteine (HC), total cholesterol (TC), triacylglycerides (TG), catalase (Cat), superoxide dismutase (SOD) and malondialdehyde (MDA).Results. When used in a model of steatohepatitis, liver function was impaired to a significantly greater extent than in the model of steatosis; this difference was manifested in a statistically significant increase in ALT, AST, AP, TC, Tbil, MDA (p &lt; 0.001) and a decrease in Cat, SOD (p &lt; 0.05). This is confirmed by the development of more pronounced symptoms of disorders of pigment and lipid metabolism, cytolytic and cholestatic syndromes, significant activation of lipid peroxidation and depression of the antioxidant system when modeling non-alcoholic steatohepatitis. Various degrees of severity of morphological changes in the experimental groups were revealed.Conclusion. The study showed the priority of determining biochemical markers, including the levels of ALT, AST, OBIL, TG, MDA and SOD to optimize laboratory methods for diagnosing the severity of liver dystrophy.The practical originality of the results lies in the optimization of the methodology for laboratory diagnosis of the severity of the pathological process in NAFLD.</p></trans-abstract><kwd-group xml:lang="ru"><kwd>неалкогольная тяжёлая болезнь печени</kwd><kwd>стеатоз печени</kwd><kwd>стеатогепатит</kwd><kwd>обмен веществ</kwd><kwd>крысы</kwd><kwd>перекисное окисление липидов</kwd><kwd>малоновый диальдегид</kwd><kwd>супероксиддисмутаза</kwd></kwd-group><kwd-group xml:lang="en"><kwd>non-alcoholic fatty liver disease</kwd><kwd>hepatic steatosis</kwd><kwd>steatohepatitis</kwd><kwd>metabolism</kwd><kwd>rats</kwd><kwd>lipid peroxidation</kwd><kwd>malondialdehyde</kwd><kwd>superoxide dismutase</kwd></kwd-group></article-meta></front><back><ref-list><title>References</title><ref id="cit1"><label>1</label><citation-alternatives><mixed-citation xml:lang="ru">Eslam M, Newsome PN, Sarin SK, Anstee QM, Targher G, Gomez MR, et al. 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