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        Aloin protects against chronic alcoholic liver injury via attenuating lipid accumulation, oxidative stress and inflammation in mice

        Yan Cui,Qing Ye,Heya Wang,Yingchao Li,Xiuhua Xia,Weirong Yao,He Qian 대한약학회 2014 Archives of Pharmacal Research Vol.37 No.12

        The present study was designed to investigatethe protective effect of aloin against alcoholic liver disease ina chronic alcohol feeding mouse model. Mice were givenalcohol twice a day by intragastric administration for11 weeks (4.0, 4.7, 5.5 g/kg bw/day for the first 3 weeksrespectively, 6.3 g/kg bw/day for the following 8 weeks). Aloin (10, 30 mg/kg bw) or vehicle was given by gavage tomice after each alcohol administration. Alcohol elevated theserum transaminases alanine aminotransferase, aspartateaminotransferase, total cholesterol and triglyceride levelswhich were significantly attenuated by the co-administrationof aloin (p\0.05). Histopathological observations wereconsistent with these indices. Co-administration of aloinsignificantly suppressed the alcohol-dependent induction ofsterol regulatory element-binding protein-1c expression(p\0.01) and remarkably up-regulated themRNA levels ofAMP-activated protein kinase-a2 (p\0.001). Furthermore,aloin supplementation significantly inhibited the alcoholdependentelevation of malondialdehyde and cytochromeP4502E1 expression (p\0.05), and significantly elevatedsuperoxide dismutase activity (p\0.01). The up-regulationof serum lipopolysaccharide (LPS), hepatic nitric oxide,tumor necrosis factor a, toll-like receptor-4, and myeloiddifferentiation primary response gene 88 were also markedlysuppressed by the co-administration of aloin (p\0.05) inalcohol-treated mice. These results suggest that aloin mayrepresent a novel, protective strategy against chronic alcoholicliver injury by attenuating lipid accumulation, oxidativestress and LPS-induced inflammatory response.

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