Вступ. Лікування хворих з приводу цирозу печінки (ЦП), печінкової недостатності та їх ускладнень, а також запального і фіброзного ураження паренхіми печінки є актуальною проблемою хірургічної гастроентерології. Ефективність діагностики й лікування дифузних захворювань печінки недостатня. Нами проведені фундаментальні дослідження для з’ясування механізмів патогенезу некрозу гепатоцитів. Матеріали і методи. На експериментальній моделі ЦП досліджені зміни концентрації проміжних продуктів ліпопероксидації та активності антиоксидантних ферментів у крові, еритроцитах, паренхімі підшлункової залози та печінки щурів. Результати. Встановлено, що формування ЦП в експерименті супроводжується накопиченням малонового діальдегіду, а також пригніченням активності антиоксидантних ферментів в крові, еритроцитах, а також паренхімі підшлункової залози та печінки щурів. Обговорення. Дисбаланс у функціональній системі ліпопероксидація – система антиоксидантного захисту - один з провідних механізмів патогенезу синдрому поліорганної недостатності при ЦП. Висновок. В комплекс патогенетично обґрунтованої корекції ЦП або печінкової недостатності слід включати препарати з антиоксидантними властивостями.
The purpose of the work was to experimentally study the chronic alcohol intoxication on the indicators of inflammation and lipid peroxidation in the gastrointestinal system. Materials and methods. Ethyl alcohol was added to the water for 2-month-old male rats, ranging from 5% to 15% for 108 days. In homogenates of mucous membranes of the gastrointestinal tract and liver, the activity of elastase enzymes, acid phosphatase and the concentration of malonic dialdehyde were determined, in serum – elastase activity and malonic dialdehyde content. Results and discussion. Biochemical research of one of the markers of inflammation (elastase activity) in rats found a probable increase of elastase activity in different parts of the digestive tract after prolonged alcohol consumption, regardless of the sex of the animals. Thus, in the serum of rats after the introduction of ethanol, the activity of elastase increased by 71.7%, in the oral mucosa – by 29.2%, in the gastric mucosa – by 55.5%, in the liver – by 29.0%. In the small and large intestine, the level of this marker of inflammation has changed slightly. The level of elastase activity shows the degree of accumulation of leukocytes in the tissues as a result of the development of the inflammatory process. Acid phosphatase activity in the oral mucosa of rats treated with ethanol increased by 47.4%, in the gastric mucosa – by 30.3%, in the mucous membrane of the small intestine – by 37.4%, in the mucous membrane of the colon – by 40.4%, in the liver – by 112.6%. Activation of acid phosphatase, along with other lysosomal enzymes, is the primary inflammatory response that triggers the production of mediators, which in turn cause secondary tissue alteration in subsequent stages of the inflammatory process. Therefore, the results obtained on the activation of acid phosphatase along with elastase indicate the presence of inflammation in the mucous membranes of the digestive tract, and especially in the liver of rats chronically treated with ethanol. The introduction of alcohol also led to an increase in the concentration of malonic dialdehyde in the mucous membranes: the oral cavity – by 20.3%, the stomach – by 32.3%, the small intestine – by 96.6%, the colon – by 50.2%, in the liver – by 39.4%, in serum – by 33.3%. A significant increase in the level of malonic dialdehyde in the tissues of the digestive tract of rats after long-term intake of ethanol is a sign of activation of lipid peroxidation and intensification of oxidative stress reactions. Conclusion. The results of the study of elastase activity indicate the development of inflammation in the mucous membranes of the gastrointestinal tract, liver and serum of rats under the influence of chronic administration of ethanol. Increased acid phosphatase activity in the tissues of the gastrointestinal tract after prolonged use of ethanol indicates damage to cell membranes, which is a consequence of inflammation. A significant increase in the level of malonic dialdehyde in the mucous membranes of the gastrointestinal tract, liver and serum of rats after chronic ethanol intake is a sign of intensification of oxidative stress reactions
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