Hepatoprotective effect of the N-alkylated isobornylamine on ССl₄ - induced liver injury in mice

Type 2 diabetes (T2D) is known to be closely associated with the development of non-alcoholic fatty liver disease (NAFLD). Therefore, it is necessary to improve liver condition concomitant to blood glucose level reduction. Previously, N-alkylated isobornylamine (compound 1) at a dose of 30 mg/kg in C57Bl/6^Ay mice was shown to resolve of fatty liver degeneration improving glucose tolerance. In this work, we carried out a study of the hepatoprotective effect of the compound 1 on ССl₄ - induced hepatotoxicity in mice. The compound 1 was administered per os to CD-1 mice at doses of 30 and 60 mg/kg daily for 3 weeks. A solution of carbon tetrachloride (0.5%) was injected 2 times a week. At the end of experiment, a biochemical blood assay was carried out, which showed that the compound 1 at both doses increased in ALT, AST and ALKP. However, total protein concentration was increased indicating a preservation of the synthetic liver function. According to the results of histological liver examination, administration of the compound 1 at doses of 30 and 60 mg/kg was found to reduce the severity of degenerative-necrotic changes in hepatocytes, while the changes at a dose of 60 mg/kg were more significant. There was a less significant polymorphism of hepatocytes and appearance of glycogen at a dose of 60 mg/kg, which may be evidence of an increased liver regeneration. Thus, isobornylamine derivative exhibit a hepatoprotective effect not only in metabolic liver injury, but also in ССl₄ - induced liver damage.