The Use of Chitosan-Coated Nanovesicles in Repairing Alcohol-Induced Damage of Liver Cells in Mice

Abstract

Background and Objectives In the past few decades, the studies concerning the natural polysaccharide chitosan have been centered on a new direction: its hepatoprotective action. The aim of our study was to evaluate the influence of previously designed chitosan lipid vesicles on the liver damage induced by alcohol consumption in mice. Materials and Methods The study involved the oral administration of substances in one daily dose as follows: Group 1 (control): water; Group 2 (control alcohol): 5% alcohol in water; Group 3 (CHIT): 0.1 mL/10 g body weight chitosan solution in animals treated with alcohol; Group 4 (CHIT-ves): 0.1 mL/10 g body chitosan vesicles in animals treated with alcohol; Group 5 (AcA): 200 mg/kg body ascorbic acid in animals treated with alcohol. In order to evaluate liver damage after alcohol consumption, the following hematological parameters were tested: the activity of alanine aminotransferase, aspartate aminotransferase and lactate dehydrogenase; serum values of urea and creatinine; the phagocytic capacity of polymorphonuclear neutrophilsin peripheral blood;serum opsonic capacity;bactericidal capacity of peritoneal macrophages; and the activity of malondialdehyde, glutathione peroxidase, superoxide dismutase and lactate dehydrogenase. Results and Conclusions The treatment with chitosan vesicles decreased liver enzyme activity and reduced the oxidative stress disturbances in alcoholic mice, thus repairing the hepatic functional and structural damages. These beneficial activities of chitosan vesicles were comparable with ascorbic acid effects in alcoholic mice.

Keywords: alcohol; chitosan; hepatoprotective; lipid vesicles; mice.

Figure 1

Chitin deacetylation into chitosan.

Figure 2

Size distribution ofchitosan solution (a) andchitosan vesicles (b).

Figure 3

Zeta potential distribution of chitosan solution (a) and chitosan vesicles (b).

Figure 4

SEM micrographs (a) and dimensional histogram (b) of the chitosan vesicles.

Figure 4

SEM micrographs (a) and dimensional histogram (b) of the chitosan vesicles.

Figure 5

The effects of chitosan, chitosan vesiclesand ascorbic acidon the activity of ALT (a), AST (b) and LDH (c) in mice. The values are expressed as mean ± S.D. of the average values for 6 animals per group. ** p < 0.01.

Figure 6

The effects of chitosan, chitosan vesiclesand ascorbic acid on the serum urea (a) and creatinine (b) levels in mice (mean ± S.D. of the average values—groups of 6 animals).

Figure 7

The effects of chitosan, chitosan vesiclesand ascorbic acid on the blood levels of OC (a), PC (b) and BC (c) in mice. The values are expressed as mean ± S.D. of the average values for 6 animals per group.

Figure 8

The effects of chitosan, chitosan vesicles and ascorbic acid on SOD (a), GPX (b) and MDA (c) activity in mice (mean ± S.D. of the average values—groups of 6 animals * p < 0.05).

Figure 9

Histopathological images of the hepatic architecture in the control (a), control alcohol (b), CHIT (c), CHIT-ves (d) and AcA (e) groups (H&E stain × 20).

Figure 10

Histopathological images of the kidney structure in the control (a), control alcohol (b), CHIT (c), CHIT-ves (d) and AcA (e) groups (H&E stain × 20).