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DOI: 10.1055/s-0034-1371829
Hepatoprotective and Antioxidant Activities of Hepacare®, a Herbal Formulation Against Carbon Tetrachloride-Induced Liver Injury
Publication History
received 09 January 2014
accepted 25 February 2014
Publication Date:
07 April 2014 (online)


Abstract
Background:
Hepacare® is a herbal formulation used to treat patients with sickle-cell anaemia complicated with jaundice, also recommended as a protective agent against liver damage due to chronic ingestion of alcohol.
Methods:
In vitro antioxidant properties of Hepacare® was determined using 1, 1- diphenyl-2-picryl-hydrazyl (DPPH), total antioxidant capacity, reducing power ability, and nitric oxide assays. Hepatoprotective effect of Hepacare® (50–400 mg/kg/day for 7 days, p.o.) was investigated in male Sprague Dawley rats against carbon tetrachloride (CCl4 /olive oil, 1:1, 0.7 ml/kg, i.p.)-induced liver damage. At the end of the study, blood samples and liver tissue were assayed for biochemical and antioxidants parameters.
Results:
Hepacare produced concentration dependent inhibition of DPPH and nitric oxide activity with IC50 of 48.50 and 55.00 µg/ml, respectively, it suppressed the absorbance of ABTS.+ with total antioxidant capacity of 423.47±8.37 mg QUE/g. CCl4 administration induced significant (P<0.001) elevation of serum aspartate transaminase (1.70 fold), alanine transaminase (1.60 fold), alkaline phosphatase (2.90 fold) and bilirubin (2.00 fold) in comparison to control. The increase in serum biomarker were dose-dependently reversed by Hepacare® pretreatment. Moreover, CCl4 pretreatment increased (P<0.001) malondialdehyde (MDA) (73.98%) and decreased (P<0.001) antioxidant enzymes level but Hepacare pretreatment produced dose-dependent attenuation of the increased MDA (3.84 fold) with enhancement of glutathione (3.08 fold), superoxide dismutase (2.08 fold), and catalase (3.14 folds) levels in comparison to CCl4 treated group, similar to those of silymarin reference standard.
Conclusion:
Hepacare was beneficial in the prevention of CCl4-induced hepatocellular injury, possibly by scavenging reactive free radicals, and boosting endogenous antioxidant systems.