Abstract
Aim:The aim of this study is to evaluate the hepatoprotective effect of rutin (RTN) in comparison to silymarin (SLM) against acetaminophen (APAP)-induced hepatotoxicity in rats.Materials and Methods:Male Wistar albino rats (n=24) of 3 months age were equally divided into four groups. Group 1 served as normal control. Hepatotoxicity was induced in the remaining three groups with administration of 500 mg/kg po APAP from day 1-3. Groups 2, 3, and 4 were subsequently administered orally with distilled water, 25 mg/kg of SLM, and 20 mg/kg of RTN, respectively, for 11 days. The mean body weights and biomarkers of hepatotoxicity were estimated on day 0, 4 (confirmation of toxicity), and 15 (at the end of treatment). Hematological parameters were evaluated on day 4 and 15. Antioxidant profile and adenosine triphosphatases (ATPases) were assessed at the end of the experiment. Liver tissues were subjected to histopathology and transmission electron microscopy after the sacrifice on day 15.Results:Antioxidant profile, ATPases, and hematological and sero-biochemical parameters were significantly altered, and histopathological changes were noticed in the liver of toxic control group. These changes were reversed in groups 3 and 4 that were administered with SLM and RTN, respectively.Conclusion:The results of the present investigation enunciated that SLM has potent hepatoprotective activity though the RTN was found superior in restoring the pathological alterations in paracetamol-induced hepatotoxicity in Wistar albino rats.
Highlights
Drug-induced hepatotoxicity accounts for the withdrawal of substantial amounts of clinically approved drugs from the market [1]
The results of the present investigation enunciated that SLM has potent hepatoprotective activity though the RTN was found superior in restoring the pathological alterations in paracetamol-induced hepatotoxicity in Wistar albino rats
APAP; paracetamol [PCM]) is a widely used overthe-counter antipyretic/analgesic agent [4,5], which is bio-activated to a reactive metabolite (N-acetyl-p-benzoquinone imine) in the liver that binds with cellular proteins covalently, deplete hepatic glutathione, and substantially cause fatal centrilobular
Summary
Drug-induced hepatotoxicity accounts for the withdrawal of substantial amounts of clinically approved drugs from the market [1]. Most of the drugs are metabolized in liver, and factors such as alcohol consumption, malnutrition, infection, and anemia affect the organ’s functional activity causing drug-induced injury [3]. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/ publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated
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