Повреждение гематоэнцефалического барьера при острых и хронических цереброваскулярных заболеваниях


И. Ианг, Г.А. Розенберг

Абстракт. Нарушение гематоэнцефалического барьера (ГЭБ) и формирование отека головного мозга играют ключевую роль в развитии патологических изменений при острой и хронической ишемии головного мозга. В исследованиях на животных обнаружили молекулярные каскады, возникающие при гипоксии клеток, образующих нейроваскулярную единицу, которые способствуют их гибели. Матриксные металлопротеиназы вызывают обратимую денатурацию белков плотных контактов в ранние сроки от начала ишемии, а позже препятствуют вторичному повреждению ГЭБ во время нейровоспалительной реакции, развивающейся спустя 24–72 часа. Циклооксигеназы препятствуют повреждению ГЭБ по мере прогрессирования нейровоспалительной реакции. Раннее повреждение ГЭБ в пределах 3-часового терапевтического окна позволяет проникнуть в мозг тканевому активатору плазминогена, что приводит к повышению риска развития кровоизлияния. Хроническая гипоксическая гипоперфузия приводит к повреждению ГЭБ, что вызывает нарушение когнитивных функций, наблюдаемых при лакунарных инсультах и поражении белого вещества головного мозга при субкортикальныой ишемии. В данном обзоре описаны изменения на молекулярном и клеточном уровнях, связанные с повреждением ГЭБ, и потенциальные методы лечения, направленные на восстановление целостности нейроваскулярной единицы.
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