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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">medsovet</journal-id><journal-title-group><journal-title xml:lang="ru">Медицинский Совет</journal-title><trans-title-group xml:lang="en"><trans-title>Meditsinskiy sovet = Medical Council</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">2079-701X</issn><issn pub-type="epub">2658-5790</issn><publisher><publisher-name>REMEDIUM GROUP Ltd.</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.21518/ms2024-197</article-id><article-id custom-type="elpub" pub-id-type="custom">medsovet-8348</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>ЗАБОЛЕВАНИЯ БИЛИАРНОЙ СИСТЕМЫ И ПЕЧЕНИ</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>DISEASES OF THE BILIARY SYSTEM AND LIVER</subject></subj-group></article-categories><title-group><article-title>Особенности системы перекисного окисления липидов – антиоксидантной защиты при неалкогольной жировой болезни печени</article-title><trans-title-group xml:lang="en"><trans-title>Traits of the lipid peroxidation – antioxidant defence system in non-alcoholic fatty liver disease</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0003-3992-9207</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Смирнова</surname><given-names>О. В.</given-names></name><name name-style="western" xml:lang="en"><surname>Smirnova</surname><given-names>O. V.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Смирнова Ольга Валентиновна, д.м.н., профессор, заведующая лабораторией клинической патофизиологии,</p><p>660022, Красноярский край, Красноярск, ул. Партизана Железняка, д. 3г</p></bio><bio xml:lang="en"><p>Olga V. Smirnova, Dr. Sci. (Med.), Professor, Head of the Laboratory of Clinical  Pathophysiology,</p><p>3g, Partizan Zheleznyak St., Krasnoyarsk, 660022</p></bio><email xlink:type="simple">ovsmirnova71@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/0000-0003-1295-9262</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Лагутинская</surname><given-names>Д. В.</given-names></name><name name-style="western" xml:lang="en"><surname>Lagutinskaya</surname><given-names>D. V.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Лагутинская Дарья Владимировна, младший научный сотрудник лаборатории клинической патофизиологии, </p><p>660022, Красноярский край, Красноярск, ул. Партизана Железняка, д. 3г</p></bio><bio xml:lang="en"><p>Darya V. Lagutinskaya, Junior Researcher of the Laboratory of Clinical Pathophysiology,</p><p>3g, Partizan Zheleznyak St., Krasnoyarsk, 660022</p></bio><email xlink:type="simple">dlagut1210@gmail.com</email><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Каспарова</surname><given-names>И. Э.</given-names></name><name name-style="western" xml:lang="en"><surname>Kasparova</surname><given-names>I. E.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Каспарова Ирина Эдуардовна, к.м.н., старший научный сотрудник лаборатории клинической патофизиологии, </p><p>660022, Красноярский край, Красноярск, ул. Партизана Железняка, д. 3г</p></bio><bio xml:lang="en"><p>Irina E. Kasparova, Cand. Sci. (Med.), Senior Researcher of the Laboratory of Clinical Pathophysiology,</p><p>3g, Partizan Zheleznyak St., Krasnoyarsk, 660022</p></bio><email xlink:type="simple">impn@impn.ru</email><xref ref-type="aff" rid="aff-1"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru"><institution>Федеральный исследовательский центр «Красноярский научный центр Сибирского отделения Российской академии наук», обособленное подразделение «Научно-исследовательский институт медицинских проблем Севера»</institution><country>Россия</country></aff><aff xml:lang="en"><institution>Federal Research Center “Krasnoyarsk Science Center of the Siberian Branch of the Russian Academy of Sciences”, Research Institute of Medical Problems of the North</institution><country>Russian Federation</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2024</year></pub-date><pub-date pub-type="epub"><day>10</day><month>06</month><year>2024</year></pub-date><volume>0</volume><issue>8</issue><fpage>116</fpage><lpage>123</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Смирнова О.В., Лагутинская Д.В., Каспарова И.Э., 2024</copyright-statement><copyright-year>2024</copyright-year><copyright-holder xml:lang="ru">Смирнова О.В., Лагутинская Д.В., Каспарова И.Э.</copyright-holder><copyright-holder xml:lang="en">Smirnova O.V., Lagutinskaya D.V., Kasparova I.E.</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.med-sovet.pro/jour/article/view/8348">https://www.med-sovet.pro/jour/article/view/8348</self-uri><abstract><sec><title>Введение</title><p>Введение. Неалкогольная жировая болезнь печени (НАЖБП) вызывается избыточным накоплением жиров в гепатоцитах. Нарастающий процент жировой ткани ассоциирован с хроническим воспалением и развивающимся оксидативным стрессом. Эти патологические состояния способны приводить к прогрессированию стеатоза в стеатогепатит с дальнейшим развитием фиброза и цирроза.</p></sec><sec><title>Цель</title><p>Цель. Оценить показатели липопероксидации и факторов антиоксидантной защиты при стеатозе и стеатогепатите у пациентов с НАЖБП.</p></sec><sec><title>Материалы и методы</title><p>Материалы и методы. В ходе работы было обследовано 116 пациентов с НАЖБП, из них 65 имели стеатоз, а 51 – стеатогепатит. Исследование биохимических маркеров патологий обмена белков, жиров и углеводов осуществлялось на биохимическом анализаторе Mindray BS-380. Оценка показателей системы «ПОЛ-АОЗ» (МДА, СОД, каталаза, церулоплазмин) осуществлялась спектрофотометрическими методами. Статистическая обработка данных осуществлялась в программах STATISTICA и SPSS 26 с помощью непараметрических критериев.</p></sec><sec><title>Результаты</title><p>Результаты. У пациентов со стеатогепатитом была более выраженная дислипидемия, уровень триглицеридов крови и общего холестерина, а также ЛПНП был значимо выше (p &gt; 0,05). Нарушение метаболизма холестерина отражал высокий ИА – 3,46. У пациентов со стеатозом изменения в липидограмме были менее выраженными. Нарушения белкового и углеводного обменов не было обнаружено. Повышение уровня печеночных маркеров было отмечено только у пациентов со стеатогепатитом. Изменение баланса в системе «ПОЛ-АОЗ» было более выражено у пациентов со стеатогепатитом, у них был высокий уровень МДА, высокая концентрация каталазы, у пациентов со стеатозом отмечалось только снижение уровня МДА и повышение уровня церулоплазмина.</p></sec><sec><title>Выводы</title><p>Выводы. Дислипидемия, цитолиз гепатоцитов и фиброз печени выявляются у больных стеатогепатитом. Нарушения в системе «ПОЛ-АОЗ» выявлены при обеих формах НАЖБП, но при стеатозе имеют компенсированный характер. При стеатогепатите нарушения «ПОЛ-АОЗ» в виде увеличения прооксидантов и снижения антиоксидантов вызывают развитие окислительного стресса.</p></sec></abstract><trans-abstract xml:lang="en"><sec><title>Introduction</title><p>Introduction. Non-alcoholic fatty liver disease (NAFLD) is caused by excess accumulation of fats in hepatocytes. An increasing percentage of adipose tissue is associated with chronic inflammation and developing oxidative stress. These pathological conditions can lead to the progression of steatosis to steatohepatitis with the further development of fibrosis and cirrhosis.</p></sec><sec><title>Aim</title><p>Aim. To evaluate the indicators of lipid peroxidation and antioxidant defence factors in steatosis and steatohepatitis in patients with NAFLD.</p></sec><sec><title>Materials and methods</title><p>Materials and methods. During the work, 116 patients with NAFLD were examined, of which 65 had steatosis, and 51 had steatohepatitis. The study of biochemical markers of metabolism of proteins, fats and carbohydrates was performed on a Mindray BS-380 biochemical analyzer. The indicators of the LPO-AOD system (MDA, SOD, catalase, ceruloplasmin) were assessed using spectrophotometric methods. Statistical data processing was carried out in the STATISTICA and SPSS 26 programs using nonparametric tests.</p></sec><sec><title>Results</title><p>Results. Patients with steatohepatitis had more severe dyslipidemia, blood triglyceride, total cholesterol levels and LDL were significantly higher (p &gt; 0.05). Impaired cholesterol metabolism was reflected by a high atherogenic index of 3.46. In patients with steatosis, changes in the lipid profile were less pronounced. No disturbances in protein and carbohydrate metabolism were detected. Increased levels of liver markers were noted only in patients with steatohepatitis. The change in the balance in the LPO- AOD system was more pronounced in patients with steatohepatitis; they had a high level of MDA, a high concentration of catalase; in patients with steatosis, only a decrease in the level of MDA and an increase in the level of ceruloplasmin were noted.</p></sec><sec><title>Conclusion</title><p>Conclusion. Dyslipidemia, hepatocyte cytolysis and liver fibrosis are detected in patients with steatohepatitis. Disturbances in the LPO-AOD system have been identified in both forms of NAFLD, but in steatosis they are compensated. In steatohepatitis, disturbances in “LPO-AOD” in the form of an increase in pro-oxidants and a decrease in antioxidants cause the development of oxidative stress.</p></sec></trans-abstract><kwd-group xml:lang="ru"><kwd>НАЖБП</kwd><kwd>стеатогепатит</kwd><kwd>дислипидемия</kwd><kwd>малоновый диальдегид</kwd><kwd>супероксиддисмутаза</kwd><kwd>каталаза</kwd><kwd>церулоплазмин</kwd><kwd>антиоксидантная защита</kwd></kwd-group><kwd-group xml:lang="en"><kwd>NAFLD</kwd><kwd>steatohepatitis</kwd><kwd>dyslipidemia</kwd><kwd>malondialdehyde</kwd><kwd>superoxide dismutase</kwd><kwd>catalase</kwd><kwd>ceruleoplasmin</kwd><kwd>antioxidant defence</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">Review Team; LaBrecque DR, Abbas Z, Anania F, Ferenci P, Khan AG, Goh KL et al.; World Gastroenterology Organisation. 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