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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="other" dtd-version="1.2" xml:lang="en"><front><journal-meta><journal-id journal-id-type="publisher-id">RUDN Journal of Medicine</journal-id><journal-title-group><journal-title xml:lang="en">RUDN Journal of Medicine</journal-title><trans-title-group xml:lang="ru"><trans-title>Вестник Российского университета дружбы народов. Серия: Медицина</trans-title></trans-title-group></journal-title-group><issn publication-format="print">2313-0245</issn><issn publication-format="electronic">2313-0261</issn><publisher><publisher-name xml:lang="en">Peoples’ Friendship University of Russia named after Patrice Lumumba (RUDN University)</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="publisher-id">3776</article-id><article-categories><subj-group subj-group-type="toc-heading" xml:lang="en"><subject>Articles</subject></subj-group><subj-group subj-group-type="toc-heading" xml:lang="ru"><subject>Статьи</subject></subj-group><subj-group subj-group-type="article-type"><subject></subject></subj-group></article-categories><title-group><article-title xml:lang="en">Inhibitors of cyclooxygenase-2-dependent modulation of functional characteristics of leukocytes</article-title><trans-title-group xml:lang="ru"><trans-title>Ингибиторы ЦОГ-2 в модуляции функциональных характеристик лейкоцитов</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author"><name-alternatives><name xml:lang="en"><surname>Pasechnik</surname><given-names>A V</given-names></name><name xml:lang="ru"><surname>Пасечник</surname><given-names>А В</given-names></name></name-alternatives><bio xml:lang="en">Кафедра общей патологии и патологической физиологииМедицинский факультет; Российский университет дружбы народов; Peoples Friendship University of Russia</bio><bio xml:lang="ru">Кафедра общей патологии и патологической физиологииМедицинский факультет; Российский университет дружбы народов</bio><email>-</email><xref ref-type="aff" rid="aff1"/></contrib><contrib contrib-type="author"><name-alternatives><name xml:lang="en"><surname>Semochkina</surname><given-names>O N</given-names></name><name xml:lang="ru"><surname>Сёмочкина</surname><given-names>О Н</given-names></name></name-alternatives><bio xml:lang="en">Кафедра общей патологии и патологической физиологииМедицинский факультет; Российский университет дружбы народов; Peoples Friendship University of Russia</bio><bio xml:lang="ru">Кафедра общей патологии и патологической физиологииМедицинский факультет; Российский университет дружбы народов</bio><email>-</email><xref ref-type="aff" rid="aff1"/></contrib><contrib contrib-type="author"><name-alternatives><name xml:lang="en"><surname>Moiseeva</surname><given-names>E G</given-names></name><name xml:lang="ru"><surname>Моисеева</surname><given-names>Е Г</given-names></name></name-alternatives><bio xml:lang="en">Кафедра общей патологии и патологической физиологииМедицинский факультет; Российский университет дружбы народов; Peoples Friendship University of Russia</bio><bio xml:lang="ru">Кафедра общей патологии и патологической физиологииМедицинский факультет; Российский университет дружбы народов</bio><email>-</email><xref ref-type="aff" rid="aff1"/></contrib></contrib-group><aff-alternatives id="aff1"><aff><institution xml:lang="en">Peoples Friendship University of Russia</institution></aff><aff><institution xml:lang="ru">Российский университет дружбы народов</institution></aff></aff-alternatives><pub-date date-type="pub" iso-8601-date="2009-01-15" publication-format="electronic"><day>15</day><month>01</month><year>2009</year></pub-date><issue>1</issue><issue-title xml:lang="en">NO1 (2009)</issue-title><issue-title xml:lang="ru">№1 (2009)</issue-title><fpage>103</fpage><lpage>105</lpage><history><date date-type="received" iso-8601-date="2016-09-07"><day>07</day><month>09</month><year>2016</year></date></history><permissions><copyright-statement xml:lang="ru">Copyright ©; 2009, Пасечник А.В., Сёмочкина О.Н., Моисеева Е.Г.</copyright-statement><copyright-year>2009</copyright-year><copyright-holder xml:lang="ru">Пасечник А.В., Сёмочкина О.Н., Моисеева Е.Г.</copyright-holder><ali:free_to_read xmlns:ali="http://www.niso.org/schemas/ali/1.0/"/><license><ali:license_ref xmlns:ali="http://www.niso.org/schemas/ali/1.0/">http://creativecommons.org/licenses/by/4.0</ali:license_ref></license></permissions><self-uri xlink:href="https://journals.rudn.ru/medicine/article/view/3776">https://journals.rudn.ru/medicine/article/view/3776</self-uri><abstract xml:lang="ru">Cyclooxygenase (COX), the primary enzyme responsible for the synthesis of prostanoids, exists in at least 2 isoforms. COX-2 has been suggested to be the isoform primarily responsible for synthesis of prostaglandins (PGs) in the context of inflammation. Thus, selective inhibitors of COX-2 were developed with the aim that they would be as effective as traditional nonsteroidal antiinflammatory drugs (NSAIDs) but would not be as damaging to the gastrointestinal tract by virtue of not inhibiting the primarily COX-1-dependent PG synthesis in those tissues. To investigate whether selective COX 2 inhibitors would play a role in a model of inflammation. The received results testify to ability of COX 2 inhibitors to increase adhesion and modulation of apoptosis and PMN free oxygen radicals production. The drugs' effect on PMN free oxygen radicals production, apoptosis and adhesion may constitute an additional mechanism of their activity. These data characterize the potential mechanism to explain effects immunomodulatory agents of pathway and therapy for inflammation, cardiovascular diseases and bronchial asthma; beta-adrenergic receptors are functionally coupled to signalling cascades in human neutrophils
These results clearly confirmed that COX-2 plays a critical role in the development of the inflammatory response by altering key components of the inflammatory cascade. Therefore, selective inhibitor of COX-2 such as celecoxib, offers a therapeutic approach for the management of various inflammatory diseases.
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