morphoМорфологические ведомостиMorphological newsletter1812-31712686-8741Private Medical University REAVIZ10.20340/mv-mn.2014.0(4):26-31morpho-342Research ArticleОРИГИНАЛЬНЫЕ ИССЛЕДОВАНИЯRESEARCH ARTICLESКЛЕТОЧНЫЕ МЕХАНИЗМЫ ХРОНИЧЕСКОГО НЕЙРОВОСПАЛЕНИЯCell mechanisms of chronic neuroinflamationСергееваТатьяна НиколаевнаSergeyevaT. N.tnbio@ya.ruСергеевВалерий ГеоргиевичSergeyevV. G.cellbio@ya.ruЧучковВиктор МихайловичChyuchkovV. M.comnayk@mail.ruФГБОУ ВПО «Удмуртский государственный университет» Минобрнауки РФRussian Federation2014301220142242631Copyright © Сергеева Т.Н., Сергеев В.Г., Чучков В.М., 20142014Сергеева Т.Н., Сергеев В.Г., Чучков В.М.Sergeyeva T.N., Sergeyev V.G., Chyuchkov V.M.Данная работа распространяется под лицензией Creative Commons Attribution 4.0.This work is licensed under a Creative Commons Attribution 4.0 License.https://www.morpholetter.com/jour/article/view/342

Нейровоспаление, которое рассматривается как ключевое звено патогенеза нейродегенеративных заболеваний, как правило, развивается задолго до гибели нейронов. Для выявления молекулярных и клеточных механизмов, обеспечивающих персистирование нейровоспаления, предшествующее нейродегенерации, мы исследовали отсроченные эффекты однократного введения бактериального эндотоксина (липополисахарида) в область черной субстанции мозга крыс. Через 8 недель, в области введения наблюдалось увеличение количества микроглиоцитов с высокой экспрессией MHC II, и астроцитов, интенсифицирующих экспрессию глиального фибриллярного кислого белка. Ярко выраженная сосудистая реакция сопровождалась индукцией синтеза в клетках стенки кровеносных сосудов фактора некроза опухоли-а, и миграцией лимфоцитов в паренхиму мозга. Полученные результаты обсуждаются с точки зрения системной организации сетевых взаимодействий между описанными клетками.

Neuroinflammation can develop long before the death of neurons. We investigated the deferred effects of a lipopolysaccharide single injection in the rat substantia nigra to identify the molecular and cellular mechanisms of persistent neuroinflammation. After 8 weeks, there was a large number of microglia and astrocytes with high expression of MHC II and glial fibrillary acidic protein, respectively. The observed reaction is accompanied by the induction tumor necrosis factor-а in the walls of blood vessels and migration of lymphocytes into the brain parenchyma. These results are discussed in terms of the systemic organization of the cells network.

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