Cell and Tissue BiologyCell and Tissue BiologyЦитология0041-37713034-6061The Russian Academy of Sciences66966710.31857/S0041377123010042GOTNXZArticlesСтатьиDisturbance in Expression of Lactate Transporters in Brain Cells under Acute Toxic Effect of Beta-Amyloid In Vitro and In VivoНарушение уровня транспортеров лактата в клетках головного мозга при остром токсическом действии бета-амилоида in vitro и in vivoGorinaYa. V.ГоринаЯ. В.yana_20@bk.ruKharitonovaE. V.ХаритоноваЕ. В.yana_20@bk.ruKhilazhevaE. D.ХилажеваЕ. Д.yana_20@bk.ruSemenovaA. A.СеменоваА. А.yana_20@bk.ruMorgunA. V.МоргунА. В.yana_20@bk.ruKomlevaYu. K.КомлеваЮ. К.yana_20@bk.ruLopatinaO. L.ЛопатинаО. Л.yana_20@bk.ruSalminaA. B.СалминаА. Б.yana_20@bk.ruResearch Institute of Molecular Medicine and Pathobiochemistry, Voino-Yasenetsky Krasnoyarsk State Medical UniversityНаучно-исследовательский институт молекулярной медицины и патобиохимии Красноярского государственного медицинского университета им. профессора В.Ф. Войно-Ясенецкого Министерства здравоохранения РФ (КрасГМУ)Department of Outpatient Pediatrics and Propaedeutics of Childhood Diseases with a Postgraduate Course, Voino-Yasenetsky Krasnoyarsk State Medical UniversityКафедра поликлинической педиатрии и пропедевтики детских болезней с курсом ПО КрасГМУCenter for Collective Use Molecular and Cellular Technologies, Voino-Yasenetsky Krasnoyarsk State Medical UniversityЦентр коллективного пользования Молекулярные и клеточные технологии, КрасГМУLaboratory of Neurobiology and Tissue Engineering, Brain Institute, Scientific Center of NeurologyЛаборатория нейробиологии и тканевой инженерии Института мозга Научного центра неврологииru010120232023651648127022025Received:27022025Published:01012023Copyright ©; 2023, Я.В. Горина, Е.В. Харитонова, Е.Д. Хилажева, А.А. Семенова, А.В. Моргун, Ю.К. Комлева, О.Л. Лопатина, А.Б. СалминаCopyright ©; 2023, Я.В. Горина, Е.В. Харитонова, Е.Д. Хилажева, А.А. Семенова, А.В. Моргун, Ю.К. Комлева, О.Л. Лопатина, А.Б. Салмина2023Я.В. Горина, Е.В. Харитонова, Е.Д. Хилажева, А.А. Семенова, А.В. Моргун, Ю.К. Комлева, О.Л. Лопатина, А.Б. СалминаЯ.В. Горина, Е.В. Харитонова, Е.Д. Хилажева, А.А. Семенова, А.В. Моргун, Ю.К. Комлева, О.Л. Лопатина, А.Б. Салминаhttps://journals.eco-vector.com/0041-3771/article/view/669667

Decreased energy metabolism in the brain correlates with cognitive impairment in Alzheimer’s disease. Accumulating experimental data indicate that lactate transporters and monocarboxylate transporters (MCTs) are directly involved in cerebral energy metabolism. However, to date, changes in lactate levels and MCT content in Alzheimer’s disease remain unclear. The aim of the study was to study the content of lactate and of its transporters – MCT1 and MCT2 in cells of neuronal, astroglial and endothelial nature under acute toxic effects of beta-amyloid (Aβ1–42) in vitro and in vivo. Under conditions of acute toxic action of Aβ1–42 in vivo, a significant (P ≤ 0.05) decrease in the level of lactate in the hippocampal tissue and an increase (P ≤ 0.05) in the dialysate were found. At the same time, a low (P ≤ 0.05) levels of MCT1 and MCT2 was set. In vitro, significantly high (P ≤ 0.05) production of lactate by astrocytes was revealed, coupled with low (P ≤ 0.05) level of MCT2 on neurons. Thus, it was found that Aβ1–42 causes a decrease in the level of lactate in the hippocampal tissue and an increase in its level in dialysate in vivo, which correlates with the impaired level of MCT1 and MCT2. This indicates a violation of energy metabolism due to the acute toxic effect of Aβ1–42. At the same time, the revealed increase in the production of lactate by astrocytes in vitro may indicate the inclusion of a compensatory mechanism aimed at maintaining the astrocyte-neuronal interaction.

Снижение энергетического метаболизма головного мозга коррелирует с когнитивными нарушениями при болезни Альцгеймера. Накапливающиеся экспериментальные данные указывают на то, что переносчики лактата и монокарбоксилатные транспортеры (МСТ) принимают непосредственное участие в церебральном энергетическом метаболизме. Однако в настоящее время изменения уровня лактата и МСТ при болезни Альцгеймера остаются неясными. Цель исследования заключалась в изучении содержания лактата и уровня его транспортеров MCT1 и MCT2 в клетках нейрональной, астроглиальной и эндотелиальной природы при остром токсическом действии бета-амилоида (Aβ1–42) in vitro и in vivo. Показано, что в условиях острого токсического действия Aβ1–42 in vivo значимо (P ≤ 0.05) уменьшается уровень лактата в ткани гиппокампа и повышается в диализате на фоне низкого уровня MCT1 и MCT2. In vitro выявлена высокая (P ≤ 0.05) продукция лактата астроцитами, сопряженная с низким (P ≤ 0.05) уровнем MCT2 на нейронах. Таким образом, Aβ1–42 вызывает снижение уровня лактата в ткани гиппокампа и повышение его уровня в диализате in vivo, что коррелирует с нарушением уровня MCT1 и MCT2. Это указывает на нарушение энергетического метаболизма за счет острого токсического действия Aβ1–42. При этом выявленное повышение продукции лактата астроцитами in vitro может свидетельствовать о включении компенсаторного механизма, направленного на поддержание астроцитарно-нейронального взаимодействия.

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