The anti-fatty liver effects of garlic oil on acute ethanol-exposed mice.
The protective effects of single dose of garlic oil (GO) on acute ethanol-induced fatty liver were investigated. Mice were treated with ethanol (4.8 g/kg bw) to induce acute fatty liver. The liver index, the serum and hepatic triglyceride (TG) levels and the histological changes were examined to evaluate the protective effects. Hepatic malondialdehyde (MDA), glutathione (GSH) levels and superoxide dismutase (SOD), glutathione reductase (GR), glutathione peroxidase (GSH-Px), glutathione-S-transferase (GST) activities were determined for the antioxidant capacity assay. Acute ethanol exposure resulted in the enlargement of the liver index and the increase of the serum and hepatic TG levels (P<0.01), which were dramatically attenuated by GO pretreatment in a dose-dependent manner (P<0.01). GO treatment (simultaneously with ethanol exposure) exhibited similar effects to those of pretreatment, while no obviously protective effects were displayed when it was used at 2h after ethanol intake. Histological changes were paralleled to these indices. Beside this, GO dramatically prolonged the drunken time and shortened the waking time, and these effects were superior to those of silymarin and tea polyphenol. In addition, GO dose-dependently suppressed the elevation of MDA levels, restored the GSH levels and enhanced the SOD, GR and GST activities. Compared with the ethanol group, the MDA levels decreased by 14.2% (P<0.05), 29.9% and 32.8% (P<0.01) in GO groups 50, 100 and 200 mg/kg, respectively. The GST activity increased by 9.97%, 19.94% (P<0.05) and 42.12% (P<0.01) of the ethanol group in GO groups 50, 100 and 200 mg/kg, respectively, while the GR activity increased by 28.57% (P<0.05), 37.97% (P<0.01), 50.45% (P<0.01) of the ethanol group in GO groups 50, 100 and 200 mg/kg, respectively. These data indicated that single dose of GO possessed ability to prevent acute ethanol-induced fatty liver, but may lose its capacity when used after ethanol exposure. The protective effects should be associated with its antioxidative activities.
Zeng
Tao
T
Institute of Toxicology, Department of Pharmacology, Shandong University, 44 Wenhua West Road, Shandong, Jinan 250012, PR China.
Guo
Fang-Fang
FF
Zhang
Cui-Li
CL
Zhao
Sheng
S
Dou
Dan-Dan
DD
Gao
Xu-Cong
XC
Xie
Ke-Qin
KQ
D000284:Administration, Oral; D000498:Allyl Compounds / Q000008:administration & dosage / Q000494:pharmacology*; D000818:Animals; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D000431:Ethanol / Q000633:toxicity*; D005234:Fatty Liver / Q000139:chemically induced* / Q000473:pathology / Q000517:prevention & control*; D005419:Flavonoids / Q000008:administration & dosage / Q000494:pharmacology; D015227:Lipid Peroxidation / Q000187:drug effects; D008099:Liver / Q000187:drug effects / Q000473:pathology; D008111:Liver Function Tests; D008297:Male; D051379:Mice; D008815:Mice, Inbred Strains; D010636:Phenols / Q000008:administration & dosage / Q000494:pharmacology; D059808:Polyphenols; D012838:Silymarin / Q000008:administration & dosage / Q000494:pharmacology; D013440:Sulfides / Q000008:administration & dosage / Q000494:pharmacology*; D013662:Tea / Q000737:chemistry; D013997:Time Factors; D014280:Triglycerides / Q000097:blood
D000498:Allyl Compounds; D005419:Flavonoids; D010636:Phenols; D059808:Polyphenols; D012838:Silymarin; D013440:Sulfides; D013662:Tea; D014280:Triglycerides; D000431:Ethanol; C038491:allyl sulfide