Effects of isoflavones on alcohol pharmacokinetics and alcohol-drinking behavior in rats
Effects of isoflavones on alcohol pharmacokinetics and alcohol-drinking behavior in rats
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DOI：
10.1093/ajcn/68.6.1512s
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发表时间：
1998-12-01
影响因子：
7.1
通讯作者：
Li, TK
中科院分区：
文献类型：
--
作者：
Lin, RC;Li, TK
葛根素、大豆苷元和大豆苷元是从葛根中分离得到的三种主要的类黄酮化合物，葛根是中国广泛使用的一种药用植物。我们研究了这些抗氧化剂对大鼠的解酒和抗异向性作用。大豆苷元和大豆苷元缩短了大鼠酒精诱导的睡眠时间（失去翻正反射），而腹腔注射乙醇的大鼠则没有。当大豆苷元与乙醇溶液一起灌胃给鼠时，血液酒精浓度（BAC）达到峰值较晚，且低于只给乙醇溶液的对照组。如果给动物喂食大豆苷，BACs的消退速度也会减慢。口服的3种异黄酮化合物没有影响肝脏酒精脱氢酶或醛脱氢酶的活性，而腹腔内给药则有报道。进一步的实验表明大豆黄酮对BAC的抑制主要是由于胃排空的延迟。所有三种化合物都抑制了嗜酒大鼠的自愿饮酒。酒精消费量的减少伴随着水摄入量的增加，因此每天消耗的液体总量保持不变。每日食物摄入量和体重增加没有受到影响。停止使用异黄酮后，酒精偏好恢复到基线水平。我们假设这些化合物对酒精强化的抑制是在大脑奖励通路中集中介导的。
Puerarin, daidzin, and daidzein are 3 major isoflavonoid compounds isolated from Pueraria lobata, an edible vine used widely in China for various medicinal purposes. We studied the antiinebriation and the antidipsotropic effects of these antioxidants in rats. Daidzin and daidzein shortened alcohol-induced sleep time (loss of righting reflex) in rats that were given ethanol intragastrically but not in those given ethanol intraperitoneally. When daidzin was given to animals intragastrically with the ethanol solution, the blood alcohol concentration (BAC) was found to peak later and be lower than in control rats that were given only the ethanol solution. BACs also receded more slowly if daidzin was fed to the animals. None of the 3 isoflavonoid compounds administered orally affected liver alcohol dehydrogenase or aldehyde dehydrogenase activities, as was reported for intraperitoneal administration. Further experiments indicated that the suppression of the BAC by daidzin was due mainly to delay of stomach emptying. All 3 compounds suppressed voluntary alcohol consumption in alcohol-preferring rats. The decrease in alcohol consumption was accompanied by an increase in water intake, so that the total volume of liquid consumed daily remained unchanged. Daily food consumption and body weight gain were not affected. Alcohol preference returned to baseline levels after the isoflavonoids were discontinued. We postulate that the suppression of alcohol reinforcement produced by these compounds is mediated centrally in the brain reward pathway.