STUDY OF THE EFFECT OF CRYOPRESERVED PLACENTA EXTRACT ON THE PROCESSES OF CYTOLYSIS AND LIPID PEROXIDATION IN CCL4-INDUCED LIVER DAMAGE

Abstract

Abstract. The search for new strategies for the correction of exogenous toxic liver lesions is due to the steady increase in the incidence of hepatitis and cirrhosis among the working population, which is an important medical and social problem. The aim is to determine the effect of cryopreserved placenta extract (CEP) on the state of the liver of rats with tetrachloromethane (CCl4)-induced damage by indicators of lipid peroxidation (LP) and markers of cytolysis. Materials and methods. Experimental studies were conducted on 28 male rats. Acute CCl4-induced hepatitis was reproduced by a single injection of 50.0% CCl4 oil solution. KEP was administered 1 time per day for 5 days before the introduction of CCl4. The material for the study was whole blood and liver homogenates, in which the content of reactants with thiobarbituric acid (TBA-RP), catalase activity, superoxide dismutase (SOD) activity, alanine aminotransferase (AlAt) and aspartate aminotransferase (AsAt) activity, as well as γ-glutamyl activity were determined. γ-glutamyl transpeptidases (γ-GTP) and alkaline phosphatase (AP) according to standard methods. Results and discussion. The study showed that the content of TBA-RP in liver homogenates was lower (p<0.01) by 35.6% in rats that were prophylactically injected with CEP compared to rats with simulated CCl4-induced hepatitis without treatment (control group). An increase in the level of catalase (p=0.02) with the use of CEP was established by 33.8% and an increase in the activity of SOD (p<0.01) by 45.5% compared to the indicators of rats in the control group. It is also shown that the level of AlAt after administration of CEP decreased (p<0.001) by 56.0%, the level of AsAt decreased (p<0.001) by 48.6%, the level of γ-HTP decreased by 37.8% compared to the rats with untreated CCl4-induced hepatitis. Conclusions. Prophylactic five-day administration of CEP leads to the leveling of CCl4-induced LP activation and signs of cytolysis syndrome.