vestimИзвестия Национальной академии наук Беларуси. Серия медицинских наукProceedings of the National Academy of Sciences of Belarus, Medical series1814-60232524-2350The Republican Unitary Enterprise Publishing House "Belaruskaya Navuka"10.29235/1814-6023-2019-16-1-108-116vestim-482Research ArticleОБЗОРЫREVIEWSМеханизмы повреждения ацинарных клеток поджелудочной железы при остром алкогольном панкреатитеMechanisms of damage of acinar pancreatic cells in acute alcohol pancreatitisМожейкоЛ. А.MozheikoL. A.

Можейко Лариса Андреевна – кандидат медицинских наук, доцент

ул. Горького, 80, 230015, г. Гродно

Larisa A. Mozheiko – Ph. D. (Med.), Assistant Professor

80, Gorky Str., 230015, Grodno

mozhejko-hist@yandex.ruГродненский государственный медицинский университетGrodno State Medical University201912032019161108116Copyright © Можейко Л.А., 20192019Можейко Л.А.Mozheiko L.A.Данная работа распространяется под лицензией Creative Commons Attribution 4.0.This work is licensed under a Creative Commons Attribution 4.0 License.https://vestimed.belnauka.by/jour/article/view/482

В обзоре представлен анализ современных сведений об основных механизмах токсичного воздействия алкоголя и его метаболитов на ацинарные клетки поджелудочной железы при остром панкреатите. Показано, что механизмы клеточного повреждения многокомпонентны и тесно взаимосвязаны регуляторными факторами молекулярного уровня. На ранней стадии заболевания они приводят к следующим структурно-функциональным изменениям ацинарных клеток, способствующим преждевременной внутриклеточной активации трипсиногена и аутоагрессии: устойчивому подъему цитозольного Ca2+ и избытку митохондриального Cа2+, дестабилизации лизосом и зимогенных гранул, нарушению аутофагии, деполяризации митохондрий, снижению выработки АТФ и некрозу.

The review analyzes the current data on the main mechanisms of toxic effects of alcohol and its metabolites on pancreatic acinar cells in acute pancreatitis. It is shown that the mechanisms of cellular damage are multicomponent and closely linked by the regulatory factors of the molecular level. At the early stage of the disease, they lead to the following structural and functional changes in acinar cells that promote the premature intracellular trypsinogen activation and autoaggression: sustained rise of cytosolic Ca2+ and excess of mitochondrial matrix Ca2+; destabilization due to lysosomes and zymogen granules; debective autophagy; mitochondrial depolarization; decreased ATP production and necrosis.

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