Dose-dependent hepatoprotective effect of emodin against acetaminophen-induced acute damage in rats
ABSTRACT 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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- "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). "
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.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 (http://www.interscience.wiley.com), 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 · 2.29 Impact Factor
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ABSTRACT: Chromosomal aberrations are frequently observed in hepatitis C virus (HCV)- and alcohol-related hepatocellular carcinomas (HCCs). The mechanisms by which chromosomal aberrations occur during hepatocarcinogenesis are still unknown. However, these aberrations are considered to be the result of deregulation of some mitotic proteins, including the alteration of Cyclin B1 and Aurora kinase A expression, and the phosphorylation of gamma-tubulin. Our study aims at investigating changes in expression of the above mentioned proteins and related intracellular pathways, in in vitro and in vivo models of both HCV- and alcohol- dependent HCCs. In this study, the molecular defects and the mechanisms involved in deregulation of the mitotic machinery were analyzed in human hepatoma cells, expressing HCV proteins treated or not with ethanol, and in liver tissues from control subjects (n=10) and patients with HCV- (n=10) or alcohol-related (n=10) HCCs. Expression of Cyclin B1, Aurora kinase A, and tyrosine-phosphorylated gamma-tubulin was analyzed in models reproducing HCV infection and ethanol treatment in HCC cells. Interestingly, HCV and alcohol increased the expression of Cyclin B, Aurora kinase A, and tyrosine-phosphorylated gamma-tubulin also in tissues from patients with HCV- or alcohol-related HCCs. In vitro models suggest that HCV requires the expression of PKR (RNA-activated protein kinase), as well as JNK (c-Jun N-terminal kinase) and p38MAPK (p38 mitogen-activated protein kinase) proteins; while, ethanol bypasses all these pathways. Our results support the idea that HCV and alcohol may promote oncogenesis by acting through the same mitotic proteins, but via different signaling pathways.Journal of Hepatology 12/2010; 54(5):956-63. DOI:10.1016/j.jhep.2010.08.016 · 10.40 Impact Factor