Abstract
The aim of the research was to assess the severity of hepatocyte apoptosis in early form of non-alcoholic fatty liver disease (NAFLD) - liver steatosis (LS). Materials and methods. Total of 83 patients of LS were examined: men 42 (50.6%), women - 41 (49.4%) at the age of 52.4 ± 12.3 years. The diagnosis of the LS was established on the basis of clinical, laboratory data, the results of ultrasound liver examination and histological examination of liver biopsy specimens. Blood plasma levels of cytokeratin-18 (CK-18) (apoptosis marker) («TPS ELISA test system», Biotech, Sweden), tumor necrotic factor alpha (TNF-α) («Human TNFα Platinum ELISA test system», "EBioscience", Austria), insulin («Insulin TEST system», USA) were examined by ELISA. The HOMA index, the NAFLD fibrosis score (NAFLD FS) were calculated. The histological activity and fibrosis were evaluated using the Brunt method. Statistics were analyzed using the "StatGraphics 2.1" , using the Mann-Whitney U test, Spearman's rank correlation analysis. Results. High content of CK-18 was found in patients with hepatic steatosis compared with that in healthy individuals - 184.4±64.6 U/l versus 90.1±37.2 U/l (p=0.030). A significant increase of laboratory markers of intrahepatic cholestasis, HOMA-IR, TNF-α, cholesterol, low-density lipoproteins, triglycerides, glucose and NAFLD FS were revealed in patients with liver steatosis relative to the control. The level of CK-18 correlated only with cholesterol in LS - r=+0,70 (p=0,004). Conclusion. An increased CK-18 level of hepatocyte apoptosis marker was detected in an early form of NAFLD - liver steatosis, indicating the risk of progression of this disease. The close relationship between the content of CK-18 and the level of cholesterol in the blood confirmed the role of the latter in the development of hepatocyte apoptosis. Therapy is aimed at arresting hepatocyte apoptosis and normalization of cholesterol levels, appropriate for the earliest form of NAFLD - liver steatosis.
Highlights
An increased CK-18 level of hepatocyte apoptosis marker was detected in an early form of non-alcoholic fatty liver disease (NAFLD) — liver steatosis, indicating the risk of progression of this disease
Therapy is aimed at arresting hepatocyte apoptosis and normalization of cholesterol levels, appropriate for the earliest form of NAFLD — liver steatosis
Molecular mechanisms of hepatic apoptosis. // Cell Death Dis. — 2014. — Vol 5 (1). — P. e996
Summary
Петрозаводск, Россия) 2 И нститут биологии — обособленное подразделение Федерального государственного бюджетного учреждения науки Федерального исследовательского центра "Карельский научный центр Российской академии наук" (ИБ КарНЦ РАН) В. апоптоз гепатоцитов при ранней форме неалкогольной жировой болезни печени. — аспирант кафедры пропедевтики внутренних болезней и гигиены Курбатова И.В. A. — post-graduate student of the department of propaedeutics of internal diseases and hygiene Kurbatova I. Цель — оценка выраженности апоптоза гепатоцитов при ранней форме неалкогольной жировой болезни печени (НАЖБП) — стеатозе печени (СП). При ранней форме НАЖБП — стеатозе печени — отмечался повышенный уровень ЦК-18 — маркера апоптоза гепатоцитов, что свидетельствовало о риске прогрессирования данного заболевания. Направленная на купирование апоптоза гепатоцитов и нормализацию уровня холестерина, целесообразна при самой ранней форме НАЖБП — стеатозе печени. Ключевые слова: неалкогольная жировая болезнь печени, стеатоз печени, апоптоз, цитокератин-18, туморнекротический фактор-альфа экспериментальная и клиническая гастроэнтерология | выпуск 157 | No 9 2018 клиническая гастроэнтерология | clinical gastroenterology
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