Abstract
The current study was undertaken to examine the possible hepatoprotective effect of natural honey against carbon tetrachloride (CCl4)-induced liver injury in mice. A significant increase in the serum aminotransferases (ALT and AST) and alkaline phosphatase activity was noticed in mice exposed to CCl4. In addition to this, a significant decrease in total antioxidant capacity and antioxidant enzymes (catalase, glutathione peroxidase and superoxide dismutase) was observed in CCl4-induction group. However, treatment with honey (400 mg/kg b.w, 4 times/ week) clearly demonstrates significant hepatoprotective activities by lowering the liver marker enzymes towards the normal reference range and restores the antioxidant enzyme levels(p<0.05). The effect of CCl4 was also noticed microscopically by alteration in liver tissue architecture. The administration of liver toxicant causes, hemorrhage, congestion, necrosis, edema and remarkable blood vessel dilation. Moreover, honey exhibited protective action against this haloalkane in tissue architecture as the severity of liver tissue alteration was significantly reduced (p<0.05). The expressional pattern of P53 protein in groups treated with CCl4 only as well as honey plus CCl4 was statistically insignificant. In conclusion, this study reveals that natural honey has a remarkable protective effect against CCl4-induced liver toxicity at antioxidant enzyme, histological and protein expression level.
Highlights
Carbon tetrachloride (CCl4) is a well-known liver toxin and its molecular mechanism behind in liver damage has been properly studied and proven satisfactorily[1]
The increase in the enzyme activities were noticed in group 4 animals (CCl4 plus honey treated group), but the level of these enzymes was markedly lesser as compared to disease control group (Figure 1)
Honey treatment significantly restored the level of these antioxidant enzymes in group 4 animals i.e. the mice intoxicated with CCl4 besides treated with honey
Summary
Carbon tetrachloride (CCl4) is a well-known liver toxin and its molecular mechanism behind in liver damage has been properly studied and proven satisfactorily[1]. The CCl4-induced liver toxicity is the main reason of hepatic dysfunction as it alters the xenobiotic metabolizing system of hepatocytes, so the common use of this haloalkane has been restricted[2] This haloalkane leads to the formation of highly toxic free radicals, accountable for attacks on unsaturated fatty acids of phospholipids present in cell membrane. The CCl4-induced liver damage is characterized by progressive tissue injury including inflammation followed by centrilobular hepatic necrosis, fibrosis as well as cirrhosis[3,4]. Exposure of this liver toxicant causes elevated reactive oxygen species (ROS) production leading to pathogenesis including degeneration of the liver and kidneys
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