diaendoСахарный диабетDiabetes mellitus2072-03512072-0378Endocrinology research centre10.14341/DM10071diaendo-10071Research ArticleОригинальные исследованияOriginal StudiesДифференциация кератиноцитов и заживление раны в стрептозотоциновой модели сахарного диабета крысы с выраженной гипергликемиейKeratinocytes differentiation and wound healing in rats with streptozotocin – induced diabetes and severe hyperglycemiahttps://orcid.org/0000-0002-3382-4458ИвановЕвгений ВикторовичIvanovEvgeniy V.

аспирант кафедры физиологии и общей патологии

PhD Student

ivanovev101@gmail.comhttps://orcid.org/0000-0002-7829-4753МорозоваМария ПавловнаMorozovaMaria P.

к.б.н., ассистент кафедры физиологии и общей патологии

PhD in Biology, assistant

mormasha@gmail.comhttps://orcid.org/0000-0002-9485-3068РжавинаЕкатерина МихайловнаRzhavinaEkaterina M.

аспирант кафедры физиологии и общей патологии

PhD Student

klochikhinaem@gmail.comhttps://orcid.org/0000-0003-2669-9457ГорбачеваАнна МаксимовнаGorbachevaAnna M.

Врач-ординатор

MD

ann.gorbachewa@yandex.ruhttps://orcid.org/0000-0002-8776-6062ГавриловаСветлана АнатольевнаGavrilovaSvetlana A.

к.б.н., доцент кафедры физиологии и общей патологии

PhD in Biology, Associate Professor

sgavrilova@mail.ruhttps://orcid.org/0000-0002-2208-5733ЕрдяковАлексей КонстантиновичErdiakovAleksei K.

кандидат биологических наук, старший научный сотрудник

PhD in Biology, Senior Researcher

hemiun@mail.ruhttps://orcid.org/0000-0001-6581-4521ГалстянГагик РадиковичGalstyanGagik R.

д.м.н., профессор

MD, PhD, Professor

galstyangagik964@gmail.comhttps://orcid.org/0000-0003-0354-5607КошелевВладимир БорисовичKoshelevVladimir B.

доктор биологических наук, профессор, зав. кафедрой физиологии и общей патологии

PhD, D.Sc., Professor

KoshelevVladimir1953@yandex.ruМосковский государственный университет имени М.В. ЛомоносоваРоссияM.V. Lomonosov Moscow State UniversityRussian FederationНациональный медицинский исследовательский центр эндокринологииРоссияEndocrinology Research CentreRussian Federation2020210420202311928Copyright © Иванов Е.В., Морозова М.П., Ржавина Е.М., Горбачева А.М., Гаврилова С.А., Ердяков А.К., Галстян Г.Р., Кошелев В.Б., 20202020Иванов Е.В., Морозова М.П., Ржавина Е.М., Горбачева А.М., Гаврилова С.А., Ердяков А.К., Галстян Г.Р., Кошелев В.Б.Ivanov E.V., Morozova M.P., Rzhavina E.M., Gorbacheva A.M., Gavrilova S.A., Erdiakov A.K., Galstyan G.R., Koshelev V.B.Данная работа распространяется под лицензией Creative Commons Attribution 4.0.This work is licensed under a Creative Commons Attribution 4.0 License.https://www.dia-endojournals.ru/jour/article/view/10071ОБОСНОВАНИЕ

ОБОСНОВАНИЕ. Сахарный диабет (СД) приводит к нарушению процессов репарации кожи, однако ведущие механизмы этой патологии до настоящего времени не выделены. В связи с этим в своей работе мы решили проверить, влияет ли гипергликемия на процесс изменения фенотипов кератиноцитов в ходе ранозаживления.

ЦЕЛЬ

ЦЕЛЬ. Изучить влияние гипергликемии на заживление раны и дифференцировку кератиноцитов в модели стрептозотоцин-индуцированного сахарного диабета крысы.

МЕТОДЫ

МЕТОДЫ. У крыс вызывали развитие СД (стрептозотоцин, 65 мг/кг, внутрибрюшинно, однократно). Рану наносили в надлопаточной области на 42-е сутки, после чего через 8, 16 и 24 сут оценивали процесс репарации с помощью гистологических методов. Иммуногистохимическим методом изучали экспрессию цитокератинов 10 и 17.

РЕЗУЛЬТАТЫ

РЕЗУЛЬТАТЫ. У крыс с СД по сравнению с контрольной группой заживление ран замедлилось на поздних этапах. В целом заживление раны сопровождалось повышением экспрессии цитокератина 10 в ее крае по сравнению с интактной кожей, у крыс с СД была нарушена активация контрактильного фенотипа кератиноцитов.

ЗАКЛЮЧЕНИЕ

ЗАКЛЮЧЕНИЕ. Гипергликемия в небольшой степени замедляет ранозаживление у крыс, препятствуя активации сократимых кератиноцитов.

BACKGROUND

BACKGROUND: Diabetes mellitus leads to disruption of the skin repair processes, but the leading mechanisms of this pathology have not yet been identified. In this regard, in our work, we decided to check how hyperglycaemia affects the process of keratinocyte phenotype changes during wound healing.

AIMS

AIMS: To study the effect of hyperglycaemia on wound healing and differentiation of keratinocytes in a rat streptozotocin-induced diabetes model.

MATERIALS AND METHODS

MATERIALS AND METHODS: Diabetes mellitus was induced in rats by using streptozotocin, 65 mg / kg, intraperitoneally, once. The wound was applied in the supra-scapular region on the 42nd day, after which (after 8, 16, and 24 days) the repair process was evaluated using histological methods. Immunohistochemistry was used to evaluate the expression of cytokeratin-10 and cytokeratin-17.

RESULTS

RESULTS: In rats with diabetes mellitus, wound healing slowed down in the later stages, compared with the control group. In general, wound healing was accompanied by an increase in the expression of cytokeratin-10 in its region compared with intact skin, and contractile keratinocytes activation was disrupted in diabetic rat wounds.

CONCLUSIONS

CONCLUSIONS: Hyperglycaemia slightly slows wound healing in rats and impairs contractile keratinocytes activation.

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The authors declare that there are no conflicts of interest present.