Особенности функционирования клеток мозга при гипергликемии и сахарном диабете

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Гипергликемия является симптомом и повреждающим фактором при сахарном диабете (СД), приводящим к системным осложнениям в организме, в том числе к макро- и микроангиопатиям головного мозга, нарушению кровоснабжения, появлению очагов нейродегенерации и запуску нейровоспаления. Нервная ткань характеризуется высоким уровнем потребления энергии и высокочувствительна к колебаниям уровня метаболических субстратов. Таким образом, крайне актуальным является исследование влияния высокого уровня глюкозы на функциональное состояние ЦНС. В обзоре предпринята попытка комплексно оценить последствия гипергликемии для клеток мозга. Анализ экспериментальных данных, полученных в in vivo и in vitro моделях СД, описывающих изменения морфофункционального состояния нейронов, микроглии и астроцитов, показал, что прямое и опосредованное влияние глюкозы в высокой концентрации зависит от типа клеток. Рецепторы и внутриклеточные сигнальные каскады астроцитов и микроглии, опосредующие действие гипергликемии и развитие нейровоспаления, могут выступать в качестве терапевтических мишеней коррекции последствий СД. Поэтому поиск способов модуляции функциональной активности глиальных клеток может оказаться эффективной стратегией для снижения тяжести последствий поражения ЦНС.

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М. П. Морозова

Российский национальный исследовательский медицинский университет им. Н. И. Пирогова

Автор, ответственный за переписку.
Email: mormasha@gmail.com

Институт физиологии

Россия, Москва

И. Г. Савинкова

Российский национальный исследовательский медицинский университет им. Н. И. Пирогова

Email: mormasha@gmail.com

Институт физиологии

Россия, Москва

Л. Р. Горбачева

Российский национальный исследовательский медицинский университет им. Н. И. Пирогова; Московский государственный университет имени М. В. Ломоносова

Email: mormasha@gmail.com

Институт физиологии

Россия, Москва; Москва

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2. Рис. 1. Основные метаболические пути, активируемые при гипергликемии и приводящие к развитию диабетической нейропатии. Условные обозначения: АФК – активные формы кислорода, ДАГ – диацилглицерол, AGE-продукты – конечные продукты глубокого гликирования, NF-κB – транскрипционный ядерный фактор каппа-В, PARP – поли(АДФ-рибозо)-полимераза, UDP-GlcNAc – уридин-дифосфат-N-ацетилглюкозамин.

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3. Рис. 2. Влияние гипергликемии на взаимодействие нейронов, астроцитов и микроглии, приводящее к нейровоспалению и нейродегенерации.

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