Institute of Nutrition, SD Model Systems of Molecular Nutrition, Friedrich-Schiller-University Jena, Jena, Germany.
Institute of Nutrition, SD Model Systems of Molecular Nutrition, Friedrich-Schiller-University Jena, Jena, Germany; Department of Nutritional Sciences, Molecular Nutritional Science, University Vienna, Vienna, Austria.
Nutrition. 2018 Jan;45:68-75. doi: 10.1016/j.nut.2017.07.010. Epub 2017 Jul 27.
Results of in vitro and in vivo studies suggest that consumption of beer is less harmful for the liver than consumption of spirits. It also has been suggested that secondary plant compounds derived from hops such as xanthohumol or iso-α-acids may have beneficial effects on the development of liver diseases of various etiologies. The aim of this study was to determine whether iso-α-acids consumed in doses achieved by "normal" beer consumption have beneficial effects on health.
Female C57 Bl/6 J mice, pretreated for 4 d with an iso-α-acid-rich extract (∼30% iso-α-acids from hops, 0.75 mg/kg body weight), were fed one bolus of ethanol (6 g/kg body weight intragastric) or an iso-caloric maltodextrin solution. Markers of liver damage, toll-like receptor-4 signaling, and lipid peroxidation were determined. Furthermore, the effect of isohumulone on the lipopolysaccharide-dependent activation of J774 A.1 macrophages, used as a model of Kupffer cells, was determined.
In the liver, acute ethanol administration led to a significant accumulation of fat (∼10-fold), which was accompanied by significantly higher inducible nitric oxide synthase protein level, elevated nitric oxide production, and increased plasminogen activator inhibitor 1 protein concentration when compared to controls. In mice pretreated with iso-α-acids, these effects of alcohol were markedly attenuated. Pretreatment of J774 A.1 macrophages with isohumulone significantly attenuated lipopolysaccharide-induced mRNA expression of inducible nitric oxide synthase and interleukin-6 as well as the release of nitric oxide.
Taken together, iso-α-acids markedly attenuated the development of acute alcohol-induced damage in mice.
体外和体内研究的结果表明，啤酒的摄入对肝脏的危害小于烈酒的摄入。此外，还有人提出，啤酒花中的次级植物化合物，如黄腐酚或异-α-酸，可能对各种病因的肝病的发展有有益的影响。本研究旨在确定通过“正常”啤酒消费摄入的异-α-酸是否对健康有有益的影响。
雌性 C57 Bl/6 J 小鼠用富含异-α-酸的提取物（来自啤酒花的约 30%异-α-酸，0.75mg/kg 体重）预处理 4 天，然后给予一剂乙醇（6g/kg 体重灌胃）或等热量麦芽糊精溶液。测定肝损伤标志物、Toll 样受体 4 信号和脂质过氧化。此外，还测定了异葎草酮对 J774 A.1 巨噬细胞（用作枯否细胞模型）依赖脂多糖激活的影响。
在肝脏中，急性乙醇给药导致脂肪显著积聚（约 10 倍），与对照组相比，诱导型一氧化氮合酶蛋白水平显著升高，一氧化氮产生增加，纤溶酶原激活物抑制剂 1 蛋白浓度升高。用异-α-酸预处理的小鼠中，酒精的这些作用明显减弱。用异葎草酮预处理 J774 A.1 巨噬细胞可显著减弱脂多糖诱导的诱导型一氧化氮合酶和白细胞介素 6 的 mRNA 表达以及一氧化氮的释放。
综上所述，异-α-酸可显著减轻小鼠急性酒精诱导损伤的发展。
