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Медицинская иммунология

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Протективные эффекты препарата нуклеотидной природы “Деринат” на течение и клеточные механизмы черепно-мозговой травмы в эксперименте

https://doi.org/10.15789/1563-0625-PEO-2392

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Аннотация

Черепно-мозговая травма является наиболее частой причиной смерти и инвалидности среди молодых людей, включая спортсменов и солдат, людей в возрасте до 45 лет в промышленно развитых странах, и представляет растущую проблему со здоровьем как в развивающихся странах, так и среди стареющих людей, лечение которых является серьезной проблемой современной медицины. Этот вид травм приводит ко многим видам расстройств и очень часто к инвалидности, что обуславливает необходимость разработки новых методов лечения травм головного мозга. В экспериментах на мышах изучали новый метод лечения травм головного мозга, в частности использовали натриевую соль дезоксирибонуклеиновой кислоты. Этот препарат известен как смесь пептидов с иммуномодулирующим действием, который широко используется для лечения воспалительных, аллергических и аутоаллергических процессов. Натриевая соль дезоксирибонуклеиновой кислоты (DNA) (Деринат), выделенная из икры русского осетра, является препаратом, эффективность применения которого  показана при лечении различных заболеваний. В настоящей работе показаны нейропротекторные, антиоксидантные и противовоспалительные эффекты «Дерината» на модели черепно-мозговой травмы (ЧМТ) у крыс. Внутрибрюшинная инъекция «Дерината» в течение 3 дней после ЧМТ снижает объем повреждения ткани мозга. Иммуногистохимический анализ позволил констатировать морфологические изменения клеток микроглии в коре головного мозга и гиппокампе через 7 дней после ЧМТ, которые значительно снижались при введении препарата, как и индуцированное ЧМТ накопление 8-оксогуанина (8-oxoG) – маркера окислительного повреждения. Для изучения клеточного механизма противовоспалительных эффектов использовали первичную культивированную мышиную микроглию с АТФ (50 мкм и 1 мм) в качестве вещества, высвобождающегося в месте повреждения, для имитации воспалительной реакции in vitro. Введение «Дерината» обуславливало повышение количества мРНК нейротрофического фактора глиальных клеток (GDNF) и фактора роста нервов (NGF) в присутствии АТФ, а уровень мРНК активатора тканевого плазминогена (tPA) снижался при действии АТФ в сочетании с «Деринатом» или без него. Хотя экспрессия мРНК интерлейкина-6 (IL6) не изменялась при действии АТФ, она возрастала при аппликации «Дерината». Те же показатели фактора-α некроза опухоли (TNFα) были значительно ингибированы. Комплекс полученных данных раскрывает механизмы иммуномодулирующего действия дезоксирибонуклеиновых кислот при ЧМТ.

Ключевые слова


Об авторах

Е. А. Корнева
ФГБНУ Институт экспериментальной медицины
Россия

Корнева Елена Андреевна - доктор медицинских наук, профессор, академик РАН, главный научный сотрудник.

197376, Санкт-Петербург, ул. Акад. Павлова, 12. Тел.: 8 (812) 234-07-24


Конфликт интересов:

нет



Е. В. Дмитриенко
ФГБНУ Институт экспериментальной медицины
Россия

Старший лаборант.

СанктПетербург


Конфликт интересов:

нет



С. Миямура
Высшая школа фармацевтических наук, Университет Кюсю
Япония

Миямура Сюнпэй – студент бакалавриата


Конфликт интересов:

нет



Н. Акимото
ФГБНУ Институт экспериментальной медицины
Япония

Акимото Нозоми – доктор наук, научный сотрудник лаборатории патофизиологии


Конфликт интересов:

нет



М. Нода
ФГБНУ Институт экспериментальной медицины
Япония

Нода Мами – доктор наук, доцент, заведующая лабораторией патофизиологии


Конфликт интересов:

нет



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Корнева Е.А., Дмитриенко Е.В., Миямура С., Акимото Н., Нода М. Протективные эффекты препарата нуклеотидной природы “Деринат” на течение и клеточные механизмы черепно-мозговой травмы в эксперименте. Медицинская иммунология. 2021;23(6):1367-1382. https://doi.org/10.15789/1563-0625-PEO-2392

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Korneva E.A., Dmitrienko E.V., Miyamura S., Noda M., Akimoto N. Protective effects of Derinat, a nucleotide-based drug, on experimental traumatic brain injury, and its cellular mechanisms. Medical Immunology (Russia). 2021;23(6):1367-1382. https://doi.org/10.15789/1563-0625-PEO-2392

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