Dose-dependent hepatoprotective effect of emodin against acetaminophen-induced acute damage in rats

Reproductive Biology and Toxicology Laboratory, School of Studies in Zoology, Jiwaji University, Gwalior 474011, India
Experimental and toxicologic pathology: official journal of the Gesellschaft fur Toxikologische Pathologie (Impact Factor: 1.86). 11/2010; 62(6):627-635. DOI: 10.1016/j.etp.2009.08.006


Protective effect of emodin (1,3,8-trihydroxy-6-methyl anthraquinone), an active compound of Ventilago madraspatana Gaertn., was evaluated against acetaminophen-induced biochemical and histological alterations in rats. Acetaminophen (2 g/kg, po) administration caused significant elevation in the release of serum transaminases, alkaline phosphatase, lactate dehydrogenase, serum bilirubin and serum protein with concomitant decrease in hemoglobin and blood sugar after 24 h of its administration. Toxicant exposure intensified the lipid peroxidation and altered glutathione status, activities of adenosine triphosphatase, acid phosphatase, alkaline phosphatase as well as major cellular constituents i.e., protein, glycogen and total cholesterol in liver and kidney. Treatment of emodin (20, 30 and 40 mg/kg, po) significantly lessened the toxicity by protecting acetaminophen-induced alterations in various blood and tissue biochemical variables after 24 h of its administration. Acetaminophen administration initiated histological damage in liver. Some degree of protection was seen after emodin therapy in a dose-dependent manner. Emodin at doses of 30 and 40 mg/kg effectively reversed toxic events induced by acetaminophen as same as silymarin (50 mg/kg, po). Thus, the study concluded that emodin at a dose of 30 mg/kg (po) possesses optimum hepatoprotective ability against acetaminophen-induced toxicity.

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    • "The hepatoprotective effects of emodin have been reported in a series of studies using animal models ( Zhang , 2006 ; Dong et al . , 2009 ; Bhadauria , 2010 ) , and some Chinese medicine compound prescriptions mainly containing rhubarb are often used for the treatment of hepatitis in clinic ( Liang et al . , 2006 ; Wang et al. , 2010 ) . "
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    ABSTRACT: Herbal medicines containing emodin, widely used for the treatment of hepatitis in clinic, have been reported with hepatotoxicity in individuals. A modest inflammatory stress potentiating liver injury has been linked to the idiosyncratic drug-induced liver injury (IDILI). In this study, we investigated the hypothesis that lipopolysaccharide (LPS) interacts with emodin could synergize to cause liver injury in rats. Emodin (ranging from 20, 40, to 80 mg/kg), which is in the range of liver protection, was administered to rats, before LPS (2.8 mg/kg) or saline vehicle treatment. The biochemical tests showed that non-toxic dosage of LPS coupled with emodin caused significant increases of plasma ALT and AST activities as compared to emodin alone treated groups (P < 0.05). In addition, with LPS or emodin alone could not induce any changes in ALT and AST activity, as compared with the control group (0.5% CMC-Na treatment). Meanwhile, the plasma proinflammatory cytokines, TNF-α, IL-1β, and IL-6 increased significantly in the emodin/LPS groups compared to either emodin groups or the LPS (P < 0.05). Histological analysis showed that liver damage was only found in emodin/LPS cotreatmented rat livers samples. These results indicate that non-toxic dosage of LPS potentiates the hepatotoxicity of emodin. This discovery raises the possibility that emodin and herbal medicines containing it may induce liver injury in the inflammatory stress even in their therapeutic dosages.
    Frontiers in Pharmacology 11/2015; 6:233. DOI:10.3389/fphar.2015.00233 · 3.80 Impact Factor
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    • "In recent years, plants essential oil (EO) and their constituents have received considerable attention due to their diverse pharmacological properties. A growing interest has been observed in the evaluation of EO for their health benefits, one of the main properties being its antioxidant activity, which enables them to attenuate the development of tumor, inflammation and liver disease (Bhadauria, 2010). EO can act as antioxidant agents by scavenging free radicals and increasing antioxidants defenses (Bakkali et al., 2008; Victoria et al., 2012). "
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    ABSTRACT: The goal of this work was to evaluate the hepatoprotector activity of Eugenia uniflora leaves essential oil in mice by the determination of the biochemical parameters: thiobarbituric acid reactive species, δ-aminulevunilate dehydratase, glutathione-S-transferase and catalase activities, non-protein thiol, and plasmatic levels of aspartate aminotransferase and alanine aminotransferase. The E. uniflora leaves essential oil (200 mg/kg) restored all of the biochemical parameters modified by the injury caused by the acetaminophen (300 mg/kg), like non-protein thiol content, δ-aminulevunilate dehydratase and glutathione-S-transferase activities on mice's liver and also decreased the levels of thiobarbituric acid reactive species on kidneys. Moreover, the increase on plasma activities aspartate aminotransferase and alanine aminotransferase was also restored by the essential oil. The exposure to acetaminophen also increased lipid peroxidation in liver and kidney. This work shows for the first time the effect of E. uniflora leaves essential oil on attenuating the injury caused by acetaminophen on mice.
    Food Bioscience 12/2013; 4:50–57. DOI:10.1016/j.fbio.2013.09.001
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    ABSTRACT: The following article from Basic & Clinical Pharmacology & Toxicology, ‘Safety Pharmacology, Acute Toxicity and Pharmacokinetics of SCP-123 and Acetaminophen’ by Donna J. Millington, Cristina Villanueva, Jason Obirek, Jean Kaufman and Christopher Smith, published online on 12 April 2010 (DOI: 10.1111/j.1742-7843.2010.00562.x) in Wiley InterScience (, has been retracted by agreement between the authors, the journal Editor in Chief, Kim Brøsen, and John Wiley and Sons A/S. The retraction has been agreed due to incorrect author affiliation.
    Basic & Clinical Pharmacology & Toxicology 04/2010; 107(2):701 - 701. DOI:10.1111/j.1742-7843.2010.00562.x · 2.38 Impact Factor
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