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<article 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" xmlns:ali="http://www.niso.org/schemas/ali/1.0/" article-type="research-article" dtd-version="1.2" xml:lang="en"><front><journal-meta><journal-id journal-id-type="publisher-id">Russian Journal of Physiology</journal-id><journal-title-group><journal-title xml:lang="en">Russian Journal of Physiology</journal-title><trans-title-group xml:lang="ru"><trans-title>Российский физиологический журнал им. И.М. Сеченова</trans-title></trans-title-group></journal-title-group><issn publication-format="print">0869-8139</issn><issn publication-format="electronic">2658-655X</issn><publisher><publisher-name xml:lang="en">The Russian Academy of Sciences</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="publisher-id">651670</article-id><article-id pub-id-type="doi">10.31857/S0869813924020022</article-id><article-id pub-id-type="edn">DJWLWB</article-id><article-categories><subj-group subj-group-type="toc-heading" xml:lang="en"><subject>EXPERIMENTAL ARTICLES</subject></subj-group><subj-group subj-group-type="toc-heading" xml:lang="ru"><subject>ЭКСПЕРИМЕНТАЛЬНЫЕ СТАТЬИ</subject></subj-group><subj-group subj-group-type="article-type"><subject>Research Article</subject></subj-group></article-categories><title-group><article-title xml:lang="en">Effect of genetically engineered drugs in aseptic necrosis of the femoral head in rats</article-title><trans-title-group xml:lang="ru"><trans-title>Влияние генно-инженерных препаратов на течение асептического некроза головки бедренной кости у крыс</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author"><name-alternatives><name xml:lang="en"><surname>Shabaldin</surname><given-names>N. А.</given-names></name><name xml:lang="ru"><surname>Шабалдин</surname><given-names>Н. А.</given-names></name></name-alternatives><address><country country="RU">Russian Federation</country></address><email>shabaldin.nk@yandex.ru</email><xref ref-type="aff" rid="aff1"/></contrib><contrib contrib-type="author"><name-alternatives><name xml:lang="en"><surname>Sinitskaya</surname><given-names>А. V.</given-names></name><name xml:lang="ru"><surname>Синицкая</surname><given-names>А. В.</given-names></name></name-alternatives><address><country country="RU">Russian Federation</country></address><email>shabaldin.nk@yandex.ru</email><xref ref-type="aff" rid="aff2"/></contrib><contrib contrib-type="author"><name-alternatives><name xml:lang="en"><surname>Igisheva</surname><given-names>L. N.</given-names></name><name xml:lang="ru"><surname>Игишева</surname><given-names>Л. Н.</given-names></name></name-alternatives><address><country country="RU">Russian Federation</country></address><email>shabaldin.nk@yandex.ru</email><xref ref-type="aff" rid="aff1"/><xref ref-type="aff" rid="aff2"/></contrib><contrib contrib-type="author"><name-alternatives><name xml:lang="en"><surname>Bogdanov</surname><given-names>L. А.</given-names></name><name xml:lang="ru"><surname>Богданов</surname><given-names>Л. А.</given-names></name></name-alternatives><address><country country="RU">Russian Federation</country></address><email>shabaldin.nk@yandex.ru</email><xref ref-type="aff" rid="aff2"/></contrib><contrib contrib-type="author"><name-alternatives><name xml:lang="en"><surname>Shabaldin</surname><given-names>А. V.</given-names></name><name xml:lang="ru"><surname>Шабалдин</surname><given-names>А. В.</given-names></name></name-alternatives><address><country country="RU">Russian Federation</country></address><email>shabaldin.nk@yandex.ru</email><xref ref-type="aff" rid="aff1"/><xref ref-type="aff" rid="aff2"/></contrib></contrib-group><aff-alternatives id="aff1"><aff><institution xml:lang="en">Kemerovo State Medical University</institution></aff><aff><institution xml:lang="ru">Кемеровский государственный медицинский университет МЗ РФ</institution></aff></aff-alternatives><aff-alternatives id="aff2"><aff><institution xml:lang="en">Research Institute for Complex Issues of Cardiovascular Diseases</institution></aff><aff><institution xml:lang="ru">НИИ комплексных проблем сердечно-сосудистых заболеваний</institution></aff></aff-alternatives><pub-date date-type="pub" iso-8601-date="2024-02-15" publication-format="electronic"><day>15</day><month>02</month><year>2024</year></pub-date><volume>110</volume><issue>2</issue><issue-title xml:lang="ru"/><fpage>169</fpage><lpage>184</lpage><history><date date-type="received" iso-8601-date="2025-02-01"><day>01</day><month>02</month><year>2025</year></date></history><permissions><copyright-statement xml:lang="en">Copyright ©; 2024, Russian Academy of Sciences</copyright-statement><copyright-statement xml:lang="ru">Copyright ©; 2024, Российская академия наук</copyright-statement><copyright-year>2024</copyright-year><copyright-holder xml:lang="en">Russian Academy of Sciences</copyright-holder><copyright-holder xml:lang="ru">Российская академия наук</copyright-holder></permissions><self-uri xlink:href="https://journals.eco-vector.com/0869-8139/article/view/651670">https://journals.eco-vector.com/0869-8139/article/view/651670</self-uri><abstract xml:lang="en"><p>Bone tissue is a dynamic structure with a metabolic function. The maintenance of bone homeostasis is carried out due to the continuous process of its renewal, remodeling. At the same time, a number of pathological processes, such as ischemic catastrophe, can lead to a violation of the balance of maintaining the constancy of the bone structure. One of these diseases is aseptic necrosis of the femoral head. The presented study analyzes the dynamics of expression of genes involved in maintaining bone tissue homeostasis, changes in the histological picture during the development of aseptic necrosis of the femoral head in laboratory rats that did not receive genetically engineered drugs and against the background of the use of inhibitors of biological action IL-6, TNF-α. After induction of aseptic necrosis in the proximal epiphysis of the femur, the histological picture in animals of different groups was not the same. More preserved bone architectonics and a larger volume of bone plates were recorded in rats receiving genetically engineered drugs compared to animals without the introduction of biological agents. The latter also had the most vivid picture of osteodestruction with increased expression of proinflammatory cytokine genes. In animals, against the background of the use of drugs of inhibitors of the biological action of IL-6, TNF-α, from the second week after induction of aseptic necrosis of the mRNA, the profile of the spongiose bone of the proximal epiphysis of the femur tended to increase the expression of osteoreparation genes. At the same time, the greatest inhibition of osteoclastogenesis gene expression was obtained in rats after injection of a monoclonal antibody to the IL-6 receptor.</p></abstract><trans-abstract xml:lang="ru"><p>Костная ткань представляет собой динамическую структуру с метаболической функцией. Поддержание гомеостаза кости осуществляется за счет непрерывного процесса ее обновления, ремоделирования. При этом ряд патологических процессов, таких как ишемическая катастрофа, могут привести к нарушению баланса поддержания постоянства костной структуры. Одним из таких заболеваний является асептический некроз головки бедренной кости. В представленном исследовании выполнен анализ динамики экспрессии генов, участвующих в поддержании гомеостаза костной ткани, изменении гистологической картины при развитии асептического некроза головки бедренной кости у лабораторных крыс, не получавших генно-инженерных препаратов и на фоне применения ингибиторов биологического действия IL-6, TNF-α. После индукции асептического некроза в проксимальном эпифизе бедренной кости гистологическая картина у животных разных групп была неодинаковой. Более сохранная костная архитектоника и больший объем костных пластинок зафиксированы у крыс, получавших генно-инженерные препараты по сравнению с животными без введения биологических агентов. У последних имела место и наиболее яркая картина остеодеструкции с усилением экспрессии генов провоспалительных цитокинов. У животных на фоне применения ингибиторов биологического действия IL-6, TNF-α со второй недели после индукции асептического некроза мРНК профиль спонгиозной кости проксимального эпифиза бедра имел тенденцию усиления экспрессии генов остеорепарации. При этом наибольшее угнетение экспрессии генов остеокластогенеза получено у крыс после инъекции моноклонального антитела к рецептору IL-6.</p></trans-abstract><kwd-group xml:lang="en"><kwd>aseptic necrosis</kwd><kwd>genetically engineered drugs</kwd><kwd>IL-6 monoclonal blocker</kwd><kwd>TNF-α inhibitor</kwd><kwd>bone homeostasis genes</kwd></kwd-group><kwd-group xml:lang="ru"><kwd>асептический некроз</kwd><kwd>генно-инженерные препараты</kwd><kwd>моноклональный блокатор IL-6</kwd><kwd>ингибитор TNF-α</kwd><kwd>гены костного гомеостаза</kwd></kwd-group><funding-group><award-group><funding-source><institution-wrap><institution xml:lang="ru">Президент Российской Федерации</institution></institution-wrap><institution-wrap><institution xml:lang="en">President of Russian Federation</institution></institution-wrap></funding-source><award-id>МК-4132.2022.3</award-id></award-group></funding-group></article-meta></front><body></body><back><ref-list><ref id="B1"><label>1.</label><mixed-citation>Смирнов АВ, Румянцев АШ (2014) Строение и функции костной ткани в норме и при патологии. 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