Protective Effects of Enicostemma littorale Blume on Oxidative Stress-Induced Liver Injury in Rats

Abstract

The hepatomodulatory response of ethanol extract of Enicostemma littorale Blume was examined in contrast to
oxidative stress-induced liver injury by carbon tetrachloride (CCl4) in albino wistar male rats. The rats received
the extract, orally at the doses of 125, 250 and 500 mg/kg b wt/day for 21 consecutive days and CCl4, at the dose
of 0.2 ml/kg b wt/twice a week, i.p with olive oil, in the ratio 1:1 treatment. The rats subjected only CCl4 with olive
oil, showed remarkable oxidative stress-induced liver injury. Supplementation of E. littorale extract significantly
(P< 0.001) increased the hepatic reduced glutathione (GSH), glutathione- s-transferase (GST), glutathione
peroxidase (GPx), superoxide dismutase (SOD), catalase (CAT) and vitamin-C (vit. C) in the liver, with a dosedependent reduction of the thiobarbituric acid reactant substances (TBARS) as evidenced by reduced hepatic
lipid peroxidation (LPO) levels, compared with the control animals. The hepatic total cholesterol and
triglycerides level were also significantly decreased in the groups receiving E. littorale extract, in comparison to
controls. Further, the hepatic marker levels-AST, ALT (aspartate and alanine transaminases), ALP (alkaline
phosphatase), ACP (acid phosphatase), -GTP (gamma glutamyl transpeptidase), LDH (lactate dehydrogenase),
SDH (sorbitol dehydrogenase), Total bilirubin, total protein and albumin in serum were also restored to normal
level dose-dependently after the supplementation of E. littorale extract in comparison to respective controls.
These biochemical observations were strongly supported by a comparative histoarchitectural examination of
liver sections from treated groups, further corroborated the hepatomodulatory role of E. littole extract. Silymarin
was used as standard drug for comparison with the E. littorale extract. In conclusion, these results suggest the
hepatomodulation by E. littorale Blume against oxidative stress mediated through interference with free radical
generation and reduction in fat metabolism