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

被引:47
作者
Bhadauria, Monika [1 ]
机构
[1] Jiwaji Univ, Sch Studies Zool, Reprod Biol & Toxicol Lab, Gwalior 474011, India
关键词
Acetaminophen; Emodin; Lipid peroxidation; Reduced glutathione; Liver marker enzymes; INDUCED HEPATOTOXICITY; BENZOQUINONE IMINE; MICE; TOXICITY; CELLS; ANTHRAQUINONE; RESVERATROL; ACTIVATION; APOPTOSIS; CANCER;
D O I
10.1016/j.etp.2009.08.006
中图分类号
R36 [病理学];
学科分类号
100104 ;
摘要
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 24h 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. (C) 2009 Elsevier GmbH. All rights reserved.
引用
收藏
页码:627 / 635
页数:9
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