Abstract

The aim of the study. To determine the effect of oligoribonucleotides-D-mannitol complexes (ORN-D-M) on the indicators of oxidative destruction of biomolecules and the antioxidant system of cells in thioacetamide (TAA)-induced liver fibrosis.Materials and methods. Liver fibrosis was induced for 8 weeks by intraperitoneal administration of TAA (150 mg/kg body weight). ORN-D-M (200 mg/kg per os) was administered orally during intoxication. At the end of the experiment, the liver was excised and examined for the content of oxidative stress products and the activity of antioxidant enzymes. Data were analyzed using the ANOVA test followed by Tukey post hoc testing.Results. It is shown that the monotherapeutic treatment of ORN-D-M in TAA-induced liver fibrosis has a pronounced protective effect, which is manifested in the reduction of oxidative stress. ORN-D-M led to the attenuation of free radical damage of biopolymers, which was manifested in a decrease in the levels of peroxidation products of lipids and proteins with a simultaneous increase in the level of protein thiol groups and reduced glutathione. In addition, treatment with complexes increased the activity of the antioxidant defence system of cells.Conclusions. The obtained results indicate that ORN-D-M complexes have a potential hepatoprotective effect in TAA-induced liver fibrosis. The complexes are able to effectively reduce the indicators of oxidative damage of biomolecules with a simultaneous increase in the activity of enzymes of the antioxidant system in TAA-induced fibrosis

Highlights

  • Liver fibrosis is a complex and dynamic process of connective tissue accumulation, which can be caused by various etiological factors [1]

  • This study showed that monotherapeutic use of oligoribonucleotides-D-mannitol complexes (ORN-D-M) from the beginning of the study and 4 weeks after the initiation of fibrosis, protects the liver from free radical oxidation, enhancing the activity of glutathione-dependent antioxidant protection

  • These results suggest that ORN-D-M may have antioxidant properties in TAA-induced liver fibrosis

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Summary

Introduction

Liver fibrosis is a complex and dynamic process of connective tissue accumulation, which can be caused by various etiological factors [1]. Excessive amounts of ROS, which are formed as a result of oxidative reactions, interfere with the normal functioning of liver cells, triggering a cascade of events leading to liver fibrosis. In this case, Kupffer cells, resident macrophages of the liver, are the main effectors that generate ROS [5]. The use of modern synthetic drugs is often accompanied by the development of side effects with prolonged use [9] This fact limits the use of chemicals and prefers drugs of natural origin

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