Abstract
Non-alcoholic steatohepatitis (NASH) is a consequence of the progression of non-alcoholic fatty liver disease (NAFLD), which can lead to cirrhosis or hepatocellular insufficiency. NAFLD is a predictor of cardiovascular diseases (CVD) development. The important factor of the latter development is atherogenic dyslipidemia, and this is a type of 20-80 % NASH patients. The objective: to study the effectiveness of platelet-enriched plasma (PRP) influence on the morpho-functional state of liver in rats with non-alcoholic steatohepatitis. Materials and methods. The study was carried out on 80 adult male Wistar rats. Animals were divided into three groups: I group - animals that received an atherogenic diet for 90 days (n=10); II group - animals with simulated NASH and DL which received a normal diet for 30 days (n=30); III group - animals with simulated NASH and DL and PRP correction (n=30); group of intact animals (n=10). NASH was simulated by introducing an atherogenic diet, which consisted of lard and 50 g / kg of butter for 90 days. PRP was punctured in the tissue of liver, twice at 0.05 ml with 7 days interval. The animals were taken out of the experiment after 90 days of the atherogenic diet and on the 30th day after its cessation or PRP injection. The indicators of body mass, liver mass index (LMI), lipogram, hepatic transaminases were determined, and the further pathological examination of the liver tissue was done. Results and discussion. On the 90th day of the atherogenic diet, the GH level was 3.19 ± 0.56 mmol/l, ALT activity was 118 ± 6.12 U/l, AST 86 ± 4.52 U/l, morphological signs of NASH were detected. On the 30th day, the lipid profile of group II rats did not have statistical differences from group I, in rats after correction of NASH with the use of PRP the level of LLD decreased by 51%, ALT activity - by 54%, AST - by 51% compared to control group (p <0.05), morphologically revealed I - II degree steatosis, focal protein dystrophy. Conclusions. On the 90th day of an atherogenic diet NASH was formed in experimental animals. They had dyslipidemia, which progressed for at least 30 days while maintaining a usual diet. After correction with PRP the level of atherogenic lipoproteins was significantly decreased in rats with NASH and DL; the activity of liver enzymes was lower compared to the group with simulated NASH and DL and the group with progression of NASH and DL for 30 days, morphologically the decrease in liver steatosis and severity of protein dystrophy comparing with a group with simulated NASH and DL and a group with progressive NASH and DL was observed for 30 days.
Highlights
Non-alcoholic fatty liver disease (NAFLD) is the most common diffuse liver disease in developed countries, where the number of patients is constantly growing [1,2]
Animals were divided into groups: Group I consisted of animals kept on an atherogenic diet for 90 days (n = 10); Group II included animals with simulated Non-alcoholic steatohepatitis (NASH) and DL, which received a normal diet for 30 days (n = 30); Group III consisted of animals with simulated NASH and DL and correction of platelet-enriched plasma (PLP) (n = 30); intact group (n = 10)
The level of high-density lipoprotein (HDL) decreased almost thrice (p = 0.000005), atherogenic index (AI) was 5.25 ± 0.36 and increased almost 5 times (p = 0) compared with the intact group; ALT activity increased almost twice (p = 0), AST - 1.5 times compared with the intact group (p = 0), glucose level increased by 130% (p = 0000002) (Table 1)
Summary
Non-alcoholic fatty liver disease (NAFLD) is the most common diffuse liver disease in developed countries, where the number of patients is constantly growing [1,2]. With a long course of NASH may aggravate the pathological process with the subsequent development of complications such as liver cirrhosis, liver failure, or hepatocellular carcinoma [6]. With prolonged dyslipidemia (DL) there is an accumulation and overload of hepatocytes with lipids with subsequent disruption of the structural organization of cells and the development of an inflammatory reaction [4,5,6]. The accumulation of lipid inclusions leads to the release of free fatty acids, activation of lipid peroxidation, proinflammatory cytokines and the development of chronic inflammation of hepatocytes, which is mediated by the release of proinflammatory cytokines [4 - 6]. DL and NASH are interrelated processes [1, 2]
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