Influence of platelet-enriched plasma on the morpho-functional state of liver in rats with induced non-alcoholic steatohepatitis and dyslipidemia
Keywordsexperimental nonalcoholic steatohepatitis, dyslipidemia, platelet-rich plasma
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.
Younossi ZM, Koenig AB, Abdelatif D, Fazel Y, Henry L, Wymer M (July 2016). "Global epidemiology of non-alcoholic fatty liver disease - Meta-analytic assessment of prevalence, incidence, and outcomes". Hepatology. 64 (1): 73–84. doi:10.1002/hep.28431.
Younossi Z, Anstee QM, Marietti M, Hardy T, Henry L, Eslam M, George J, Bugianesi E (January 2018). "Global burden of NAFLD and NASH: trends, predictions, risk factors and prevention". Nature Reviews. Gastroenterology & Hepatology. 15 (1): 11–20. doi:10.1038/nrgastro.2017.109. PMID 28930295.
van den Berg E. H., Douwes R. M., de Meijer V. E., Schreuder T. C., Blokzijl H. Liver transplantation for NASH cirrhosis is not performed at the expense of major post-operative morbidity. Digestive and Liver Disease. 2018;50(1):G68–G75. doi: 10.1016/j.dld.2017.08.022
Newsome PN, Allison ME, Andrews PA, etal. Guidelines for liver transplantation for patients with non-alcoholic steatohepatitis/ Gut 2012;61:484-500.
Kanda T, Matsuoka S, Yamazaki M, Shibata T, Nirei K, Takahashi H et al. Apoptosis and non-alcoholic fatty liver diseases. World J. Gastroenterol. 2018. Jul:24(25);2661-72 p. doi: 10.3748.
Marengo A, Rosso C, Bugianesi E (14 January 2016). "Liver Cancer: Connections with Obesity, Fatty Liver, and Cirrhosis". Annual Review of Medicine. 67 (1): 103–17. doi:10.1146/annurev-med-090514-013832.
Guideline on the Management of Blood Cholesterol: A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Clinical Practice Guidelines. J Am CollCardiol 2018;Nov 10
Friedman SL, Neuschwander-Tetri BA, Rinella M, Sanyal AJ (July 2018). "Mechanisms of NAFLD development and therapeutic strategies". Nature Medicine. 24 (7): 908–922. doi:10.1038/s41591-018-0104-9.
Wang HH, Garruti G, Liu M, Porthincasa D, Wang DQ. Cholesterol and lipoprotein metabolism and atherosclerosis: recent advances in reverse cholesterol transport. Ann Hepatol. Nov. 2017:16(Suppl. 1: s3-105.); s27-s.42p. doi:10.5604/01.3001.0010.5495.
Mancini GB, Tashakkor AY, Baker S, Bergeron J, Fitchett D, Frohlich J, Genest J, Gupta M, Hegele RA, Ng DS, Pearson GJ, Pope J (December 2013). "Diagnosis, prevention, and management of state in adverse effects and intolerance: Canadian Working Group Consensus update". The Canadian Journal of Cardiology. 29 (12): 1553–68. doi:10.1016.
Shwetha Hulimavu Ramaswamy Reddy, Roopa Reddy, N Chaitanya Babu, G N Ashok Stem-cell therapy and platelet-rich plasma in regenerative medicines: A review on pros and cons of the technologies. Oral Maxillofac Pathol. 2018 Sep-Dec; 22(3): 367–374. doi: 10.4103/jomfp.JOMFP_93_18
Afsa eh Mafi, Farzaneh Dehghani, Abbas Moghadam, Ali Noorafshan, Zahra Vojdani & Tahereh Talaei-Khozani (2016) Effects of platelet-rich plasma on liver regeneration in CCl4-induced hepatotoxicity model, Platelets, 27:8, 771-776, DOI: 10.1080/09537104.2016.1184749
Shoeib HM, Keshk WA, Foda AM, Abo El Noeman SEAE. A study on the regenerative effect of platelet-rich plasma on experimentally induced hepatic damage in albino rats. Can J Physiol Pharmacol. 2018 Jun;96(6):630-636. doi:10.1139/cjpp-2017-0738.
Salem N, Hamza A, Alnahdi H, Ayaz N. Biochemical and molecular mechanisms of platelet-rich plasma in ameliorating liver fibrosis induced by dimethyl nitrosurea. Cell Physiol Biochem. 2018;47:2331–2339. doi:10.1159/000491544.
How to Cite
The periodical offers access to content in the Open Access system under the Creative Commons Attribution-NonCommercial-ShareAlike 4.0
Number of views and downloads: 136
Number of citations: 0