Effect of Curcumin on Hepatic Antioxidant Enzymes Activities and Gene Expressions in Rats Intoxicated with Aflatoxin B1

被引:103
|
作者
El-Bahr, S. M. [1 ,2 ]
机构
[1] King Faisal Univ, Dept Physiol, Coll Vet Med & Anim Resources, Biochem & Pharmacol Biochem, King, WI, Saudi Arabia
[2] Univ Alexandria, Dept Biochem, Fac Vet Med, Alexandria, Egypt
关键词
liver damage; Curcuma longa; antioxidants; oxidative stress; biomarkers; INDUCED LIPID-PEROXIDATION; HEPATOCELLULAR-CARCINOMA; LIVER; MICE; B-1; KIDNEY; INHIBITION; COMPONENT; DAMAGE; LONGA;
D O I
10.1002/ptr.5239
中图分类号
R914 [药物化学];
学科分类号
100701 ;
摘要
Twenty-eight rats were examined in a 5-week experiment to investigate the effect of curcumin on gene expression and activities of hepatic antioxidant enzymes in rats intoxicated with aflatoxin B1 (AFB(1)). The rats were divided into four groups. Rats in 1-4 groups served as control, oral curcumin treated (15mg/kg body weight), single i.p. dose of AFB(1) (3mg/kg body weight) and combination of single i.p. dose of AFB(1) with oral curcumin treated, respectively. AFB(1) Liver damage and oxidative stress were evident in untreated AFB(1)-intoxicated rats as indicated by a significant elevation in hepatic transaminases, elevation in lipid peroxide biomarkers (thiobarbituric acid reactive substances; TBARS), reduction of reduced glutathione (GSH) concentration, reduction in the activities of antioxidant enzymes namely catalase (CAT), total superoxide dismutase (SOD), glutathione peroxidase (GPX) and glutathione-S-transferase (GST) and down-regulation of gene expression of these antioxidant enzymes compared to control. Liver sections of rats intoxicated with AFB(1) showed a disrupted lobular architecture, scattered necrotic cells and biliary proliferation. Administration of curcumin with AFB(1) resulted in amelioration of AFB(1)-induced effects compared to untreated AFB(1)-intoxicated rats via an up-regulation of antioxidant enzyme gene expression, activation of the expressed genes and increase in the availability of GSH. Copyright (c) 2014 John Wiley & Sons, Ltd.
引用
收藏
页码:134 / 140
页数:7
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