Zingiber officinale Roscoe prevents acetaminophen-induced acute hepatotoxicity by enhancing hepatic antioxidant status

被引:100
作者
Ajith, T. A. [1 ]
Hema, U. [1 ]
Aswathy, M. S. [1 ]
机构
[1] Amala Inst Med Sci, Dept Biochem, Kerala 680555, India
关键词
antioxidant; free radicals; hepatotoxicity; Zingiber officinale;
D O I
10.1016/j.fct.2007.06.001
中图分类号
TS2 [食品工业];
学科分类号
0832 ;
摘要
A large number of xenobiotics are reported to be potentially hepatotoxic. Free radicals generated from the xenobiotic metabolism can induce lesions of the liver and react with the basic cellular constituents - proteins, lipids, RNA and DNA. Hepato protective activity of aqueous ethanol extract of Zingiber officinale was evaluated against single dose of acetaminophen-induced (3 g/kg, p.o.) acute hepatotoxicity in rat. Aqueous extract of Z. officinale significantly protected the hepatotoxicity as evident from the activities of serum transaminase and alkaline phosphatase (ALP). Serum glutamate pyruvate transaminase (SGPT), serum glutamate oxaloacetate transaminase (SGOT) and ALP activities were significantly (p < 0.01) elevated in the acetaminophen alone treated animals. Antioxidant status in liver such as activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase and glutathione-S-transferase (GST), a phase II enzyme, and levels of reduced glutathione (GSH) were declined significantly (p < 0.01) in the acetaminophen alone treated animals (control group). Hepatic lipid peroxidation was enhanced significantly (p < 0.01) in the control group. Administration of single dose of aqueous extract of Z. officinale (200 and 400 mg/kg, p.o.) prior to acetaminophen significantly declines the activities of serum transaminases and ALP. Further the hepatic antioxidant status was enhanced in the Z. officinale plus acetaminophen treated group than the control group. The results of the present study concluded that the hepatoprotective effect of aqueous ethanol extract of Z officinale against acetaminophen-induced acute toxicity is mediated either by preventing the decline of hepatic antioxidant status or due to its direct radical scavenging capacity. (C) 2007 Elsevier Ltd. All rights reserved.
引用
收藏
页码:2267 / 2272
页数:6
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