Authors: Yan Cui Qing Ye Heya Wang Yingchao Li Xiuhua Xia Weirong Yao He Qian
Publish Date: 2014/03/27
Volume: 37, Issue: 12, Pages: 1624-1633
Abstract
The present study was designed to investigate the protective effect of aloin against alcoholic liver disease in a chronic alcohol feeding mouse model Mice were given alcohol twice a day by intragastric administration for 11 weeks 40 47 55 g/kg bw/day for the first 3 weeks respectively 63 g/kg bw/day for the following 8 weeks Aloin 10 30 mg/kg bw or vehicle was given by gavage to mice after each alcohol administration Alcohol elevated the serum transaminases alanine aminotransferase aspartate aminotransferase total cholesterol and triglyceride levels which were significantly attenuated by the coadministration of aloin p 005 Histopathological observations were consistent with these indices Coadministration of aloin significantly suppressed the alcoholdependent induction of sterol regulatory elementbinding protein1c expression p 001 and remarkably upregulated the mRNA levels of AMPactivated protein kinaseα2 p 0001 Furthermore aloin supplementation significantly inhibited the alcoholdependent elevation of malondialdehyde and cytochrome P4502E1 expression p 005 and significantly elevated superoxide dismutase activity p 001 The upregulation of serum lipopolysaccharide LPS hepatic nitric oxide tumor necrosis factor α tolllike receptor4 and myeloid differentiation primary response gene 88 were also markedly suppressed by the coadministration of aloin p 005 in alcoholtreated mice These results suggest that aloin may represent a novel protective strategy against chronic alcoholic liver injury by attenuating lipid accumulation oxidative stress and LPSinduced inflammatory responseThis work was supported by the National Science and Technology Support Program in the 12th 5 year Plan of China No 2011BAZ02169 the Priority Academic Program Development of Jiangsu Higher Education Institution PAPD and the Fundamental Research Funds for the Central Universities of China No JUDCF10057 JUSRP11121
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