Abstract
The current study aimed to evaluate the probable protective effect of Lepidium sativum seeds (LSS) against CCl4 induced hepatic injury in New-Zealand rabbits. Rabbits were randomly divided into two main groups; group-A (noninjured group, n=15) was divided to subgroups A1 (untreated control) and A2 and A3 which received 200 & 400 mg/kg bw of LSS, respectively, in their diet daily. Group-B (injured group, n=30) were subcutaneously injected with CCl4 (0.5 ml/kg bw) starting from day one of the experiment and were equally divided into 3 subgroups: B1 received normal standard diet and B2 & B3 received 200 & 400 mg/kg bw of LSS, respectively, in their diet daily. Five rabbits of all subgroups were decapitated 5 and 10 weeks after experimental running. Biochemical analysis revealed significant decrease in serum levels of transaminases, γ-GT, ALP, total bilirubin, cholesterol, triglycerides associated with significant increase in the serum levels of T protein and albumin of 200 and 400 mg/kg bw of LSS protected rabbits for 5 and 10 weeks as compared with CCl4 treated rabbits. Oxidative stress and depressed antioxidant system of the liver tissues were markedly obvious in the CCl4 treated group. LSS administration reversed these results towards normalization. Histopathological examination of LSS protected rabbits (200 mg/kg bw of LSS for 10 weeks) showed improvement of the histoarchitectural changes of the liver induced by CCl4 to the normal aspect, showing regenerating hepatocytes with no steatosis, discrete chronic venous congestion, and discrete inflammatory infiltrate. The current findings provide new evidence that LSS could reverse the hepatotoxic effects of CCl4 and repair the liver functions.
Highlights
Carbon tetrachloride (CCl4) is a xenobiotic industrial solvent that is used to induce chemical hepatitis and liver injuries in experimental animals
Lepidium sativum seed analysis by GC/MS exhibited the presence of high concentrations of mainly α-linolenic acid (ALA) which is n−3 fatty acid, an omega-3 fatty acid found in seeds exerting its bioactivity in ameliorating the hepatic intoxication and oxidative stress including liver injury induced by alcohol [30], liver steatosis [31, 32], nonalcoholic hepatic disease [33], and parenteral nutrition-associated liver disease [34]
The results of the current study revealed that the exposure to CCl4 for 5 and 10 weeks led to a significant decrease in the enzymatic activities of CAT, GPx, Glutathione reductase (GR), GST, and Super-oxide dismutase (SOD) in the liver homogenate of CCl4 treated rabbits 5 and 10 weeks after experimental running compared to those of the normal control
Summary
Carbon tetrachloride (CCl4) is a xenobiotic industrial solvent that is used to induce chemical hepatitis and liver injuries in experimental animals. Carbon tetrachloride-induced liver injuries are the most common experimental model for monitoring the hepatoprotective activity of certain drugs. Mechanistic studies offer evidence that metabolism of CCl4 via CYP2E1 to strongly reactive free radical metabolites plays a crucial role in the proposed mode of action. The major metabolites, trichloromethyl (CCl3⋅) and trichloromethyl peroxy (CCl3O2⋅) free radicals, are extremely reactive and are capable of covalent bind to cellular macromolecules, preferring fatty acids of the membrane phospholipids. The free radicals induce cell membrane lipid peroxidation via disrupting polyunsaturated fatty acids within these membranes, initiating a sequential free radical chain reaction [1]
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