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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">helmholtzeyeinstitute</journal-id><journal-title-group><journal-title xml:lang="ru">Российский офтальмологический журнал</journal-title><trans-title-group xml:lang="en"><trans-title>Russian Ophthalmological Journal</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">2072-0076</issn><issn pub-type="epub">2587-5760</issn><publisher><publisher-name>Real time Publishers</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.21516/2072-0076-2022-15-4-72-76</article-id><article-id custom-type="elpub" pub-id-type="custom">helmholtzeyeinstitute-1101</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>КЛИНИЧЕСКИЕ ИССЛЕДОВАНИЯ</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>CLINICAL STUDIES</subject></subj-group></article-categories><title-group><article-title>Роль медиаторов врожденного иммунитета в индукции нейродегенерации сетчатки при сахарном диабете 2-го типа</article-title><trans-title-group xml:lang="en"><trans-title>The role of innate immune system mediators in the development of retinal neurodegeneration in type 2 diabetes mellitus</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-8966-3120</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Ручкин</surname><given-names>М. П.</given-names></name><name name-style="western" xml:lang="en"><surname>Ruchkin</surname><given-names>M. P.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Михаил Петрович Ручкин — аспирант кафедры нормальной и патологической физиологии, заведующий диагностическим отделением</p><p>пр-т Острякова, д. 2, Владивосток, 690002</p><p>ул. Борисенко, д. 100Е, Владивосток, 690000</p></bio><bio xml:lang="en"><p>Mikhail P. Ruchkin — PhD student, chair of normal and pathological physiology, head of diagnostic department</p><p>2, Ostryakova Ave., Vladivostok, 690002</p><p>100E, Borisenko St., Vladivostok, 690000</p></bio><email xlink:type="simple">michaelr-n@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/0000-0001-6632-9800</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Маркелова</surname><given-names>Е. В.</given-names></name><name name-style="western" xml:lang="en"><surname>Markelova</surname><given-names>E. V.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Елена Владимировна Маркелова — д-р мед. наук, профессор, заведующая кафедрой нормальной и патологической физиологии</p><p>пр-т Острякова, д. 2, Владивосток, 690002</p></bio><bio xml:lang="en"><p>Elena V. Markelova — Dr. of Med. Sci., professor, head of chair of normal and pathological physiology</p><p>2, Ostryakova Ave., Vladivostok, 690002</p></bio><xref ref-type="aff" rid="aff-2"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Федяшев</surname><given-names>Г. А.</given-names></name><name name-style="western" xml:lang="en"><surname>Fedyashev</surname><given-names>G. A.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Глеб Арнольдович Федяшев — д-р мед. наук, профессор кафедры офтальмологии и оториноларингологии, главный врач</p><p>пр-т Острякова, д. 2, Владивосток, 690002</p><p>ул. Борисенко, д. 100Е, Владивосток, 690000</p></bio><bio xml:lang="en"><p>Gleb A. Fedyashev — Dr. of Med. Sci., professor, chair of ophthalmology and otorhinolaryngology, chief physician</p><p>2, Ostryakova Ave., Vladivostok, 690002</p><p>100E, Borisenko St., Vladivostok, 690000</p></bio><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Красников</surname><given-names>В. Е.</given-names></name><name name-style="western" xml:lang="en"><surname>Krasnikov</surname><given-names>V. E.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Владимир Егорович Красников — канд. мед. наук, доцент кафедры нормальной и патологической физиологии</p><p>пр-т Острякова, д. 2, Владивосток, 690002</p></bio><bio xml:lang="en"><p>Vladimir E. Krasnikov — Cand. of Med. Sci., assistant professor, chair of normal and pathological physiology</p><p>2, Ostryakova Ave., Vladivostok, 690002</p></bio><xref ref-type="aff" rid="aff-2"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru"><institution>ФГБОУ ВО «Тихоокеанский государственный медицинский университет» Минздрава России; ООО «Приморский центр микрохирургии глаза»</institution><country>Россия</country></aff><aff xml:lang="en"><institution>Pacific State Medical University; Primor’ye center of eye microsurgery</institution><country>Russian Federation</country></aff></aff-alternatives><aff-alternatives id="aff-2"><aff xml:lang="ru"><institution>ФГБОУ ВО «Тихоокеанский государственный медицинский университет» Минздрава России</institution><country>Россия</country></aff><aff xml:lang="en"><institution>Pacific State Medical University</institution><country>Russian Federation</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2022</year></pub-date><pub-date pub-type="epub"><day>14</day><month>12</month><year>2022</year></pub-date><volume>15</volume><issue>4</issue><fpage>72</fpage><lpage>76</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Ручкин М.П., Маркелова Е.В., Федяшев Г.А., Красников В.Е., 2022</copyright-statement><copyright-year>2022</copyright-year><copyright-holder xml:lang="ru">Ручкин М.П., Маркелова Е.В., Федяшев Г.А., Красников В.Е.</copyright-holder><copyright-holder xml:lang="en">Ruchkin M.P., Markelova E.V., Fedyashev G.A., Krasnikov V.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://roj.igb.ru/jour/article/view/1101">https://roj.igb.ru/jour/article/view/1101</self-uri><abstract><p>Цель работы — определить уровень трансформирующих факторов роста-β (TGF- β1, TGF- β2, TGF- β3), интерферона-ʏ (INF- ʏ), матриксной металлопротеиназы-9 (ММP-9) и белка S100B в сыворотке крови у пациентов с сахарным диабетом (СД) 2-го типа и выявить взаимосвязь этих показателей с нейродегенеративными изменениями в сетчатке. Материал и методы. Тридцать пациентов (средний возраст — 63,5 года) с СД 2-го типа без клинических признаков диабетической ретинопатии (ДР) (основная группа) и 30 практически здоровых лиц (средний возраст — 60,3 года) (группа контроля) были обследованы с помощью микропериметрии и оптической когерентной томографии. Методом сэндвич-варианта твердофазного иммуноферментного анализа в сыворотке крови обследованных определяли уровень TGF- β1, TGF- β2, TGF- β3, INF- ʏ, ММР-9 и белка S100B. Результаты. У пациентов с СД 2-го типа выявлено увеличение объема фокальных потерь ганглиозных клеток сетчатки (ГКС) и уменьшение средней светочувствительности сетчатки. В этой группе обнаружено достоверное увеличение уровня белка S100B, а также сывороточного уровня MMP-9 по ср авнению с контролем, однако значимой разницы между группами в уровне TIMP-1 не отмечено. Уровень TGF- β2 был достоверно выше у пациентов основной группы, у этих пациентов был также выявлен дефицит TGF- β3. Не зарегистрировано достоверной разницы между группами по уровню TGF- β1 и INF- ʏ. Выявлена положительная корреляция между уровнем белка S100B, уровнем MMP-9 и объемом фокальных потерь ГКС. Заключение. У пациентов с СД 2-го типа и признаками нейродегенерации сетчатки повышена активность некоторых цитокинов и ММP-9. Это может свидетельствовать о значительной роли нейровоспаления и дисфункции иммунной системы в процессе нейродегенерации сетчатки при СД. Требуется дальнейшее наблюдение и исследование других цитокинов для определения ранних и более чувствительных маркеров нейродегенерации сетчатки.</p></abstract><trans-abstract xml:lang="en"><p>Purpose. To detect the levels of transform growth factors-β (TGF- β1, TGF- β2, TGF- β3), interferon-ʏ (INF- ʏ), matrix metalloproteinase-9 (MMP-9) and S100B protein in blood serum of patients with type 2 diabetes mellitus (DM) and to reveal the connection of these factors with neurodegenerative changes in the retina. Material and methods. 30 patients, averagely aged 60.3, with type 2 DM and no signs of diabetic retinopathy (DR) (the main group) and 30 healthy individuals (control group) were examined using microperimetry and optical coherence tomography. A sandwich variance estimator of solid phase enzyme-linked immunosorbent assay was used to determine the levels of TGF- β 1, TGF- β2, TGF- β3, INF- ʏ, ММР-9 and S100B protein in blood serum of the subjects examined. Results. The patients with type 2 DM were found to experience an increased level of focal loss of retinal ganglion cells and a drop in the average photosensitivity of the retina. The main group also showed a reliable increase in the level of S100B protein and in the serum level of MMP-9 against the control, but no significant difference between the groups was found in the level of TIMP-1. The level of TGF- β2 was significantly higher in the main group, which also showed a deficiency of TGF- β3. No significant difference was found between the two groups in the levels of TGF- β1 or INF- ʏ. In contrast, a positive correlation was revealed between the levels of S100B, MMP-9 and the volume of focal loss of retinal ganglion cells. Conclusion. Patients with type 2 DM and signs of neurodegeneration of the retina reveal a higher activity of some cytokines and MMP-9. This may indicate an important role of neuroinflammation and dysfunction of the immune system in the retinal neurodegeneration process of DM patients. Further research of other cytokins is required to determine early and more sensitive markers of retinal neurodegeneration. </p></trans-abstract><kwd-group xml:lang="ru"><kwd>диабетическая ретинопатия</kwd><kwd>сахарный диабет</kwd><kwd>нейродегенерация</kwd><kwd>цитокины</kwd><kwd>матриксные металлопротеиназы</kwd></kwd-group><kwd-group xml:lang="en"><kwd>diabetic retinopathy</kwd><kwd>diabetes mellitus</kwd><kwd>neurodegeneration</kwd><kwd>cytokines</kwd><kwd>matrix metalloproteinases</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">Khan A., Hashim M., King J., et al. Epidemiology of type 2 diabetes – global burden of disease and forecasted trends. Epidemiol. Glod. Health. 2020; 10 (1): 107–11. doi:10.2991/jegh.k.191028.001</mixed-citation><mixed-citation xml:lang="en">Khan A., Hashim M., King J., et al. 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