Protective Effect of Daidzin against D-Galactosamine and Lipopolysaccharide-Induced Hepatic Failure in Mice

被引:26
作者
Kim, Sung-Hwa [1 ]
Heo, Jeong-Haing [1 ]
Kim, Yeong Shik [2 ]
Kang, Sam Sik [2 ]
Choi, Jae Sue [3 ]
Lee, Sun-Mee [1 ]
机构
[1] Sungkyunkwan Univ, Coll Pharm, Suwon 440746, Gyeonggi Do, South Korea
[2] Seoul Natl Univ, Coll Pharm, Seoul 110460, South Korea
[3] Pukyong Natl Univ, Fac Food Sci & Biotechnol, Pusan 608737, South Korea
关键词
apoptosis; daidzin; D-galactosamine; LPS; liver failure; oxidative stress; TNF-alpha; PERMEABILITY TRANSITION PORE; ISCHEMIA-REPERFUSION; PUERARIAE RADIX; LIVER-DAMAGE; MITOCHONDRIAL; GLUTATHIONE; APOPTOSIS; MECHANISMS; INJURY; POTENT;
D O I
10.1002/ptr.2710
中图分类号
R914 [药物化学];
学科分类号
100701 ;
摘要
This study examined the effects of daidzin, a major isoflavone from Puerariae Radix, on D-galactosamine (D-GalN) and lipopolysaccharide (LPS)-induced liver failure. Mice were given an intraperitoneal injection of daidzin (25, 50, 100 and 200 mg/kg) 1 h before receiving an injection of D-GalN (700 mg/kg)/LPS (10 mu g/kg). Daidzin markedly reduced the elevated serum aminotransferase activity and the levels of lipid peroxidation and tumor necrosis factor-alpha. The glutathione content was lower in the D-GalN/LPS group, which was attenuated by daidzin. The daidzin pretreatment attenuated the swollen mitochondria observed in the D-GalN/LPS group. Daidzin attenuated the apoptosis of hepatocytes, which was confirmed using the terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling method and a caspase-3 assay. Overall, these results suggest that the liver protection of daidzin is due to reduced oxidative stress and its antiapoptotic activity. Copyright (C) 2008 John Wiley & Sons, Ltd.
引用
收藏
页码:701 / 706
页数:6
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