魔芋葡甘聚糖抗醉解酒作用机理研究

摘要

以不同剂量的魔芋葡甘露聚糖(Konjac Glucomannan,KGM)灌胃昆明种小鼠,采用56%vol红星二锅头灌胃方法进行造模,研究KGM对小鼠的抗醉解酒作用及机理.结果表明:中(240 mg/kg)、高(400 mg/kg)剂量组可有效延长醉酒潜伏期,显著缩短醉酒小鼠的睡眠时间和醒酒时间,且高、中剂量组的血清乙醇浓度显著低于模型组小鼠,高剂量组小鼠肝组织匀浆中乙醇脱氢酶(Alcohol dehydrogenase,ADH)、乙醛脱氢酶(Acetaldehyde dehydrogenase,ALDH)和细胞色素P450(Cytochrome P450,P450)含量均显著升高;中、高剂量组小鼠胃黏膜组织和血清中丙二醛(Methane dicarboxylic aldehyde,MDA)含量显著降低,过氧化物歧化酶(Superoxide Dismutase,SOD)活力、一氧化氮(Nitric Monoxide,NO)含量、前列腺素 E2(Prostaglandin E,PGE2)含量显著升高.其解酒机理: ①可能是其抑制酒精的吸收,降低血清中乙醇浓度;② 小鼠胃黏膜和血清中MDA含量的降低,SOD活力、NO 和 PGE 的升高减轻了酒精对胃黏膜的损伤,并提高了肝脏中ADH、ALDH、P450含量,通过乙醇脱氢酶和乙醇氧化酶系统加速酒精代谢,发挥其防醉解酒作用.%In this study, different doses of konjac gum powder (KGM) were administered to Kunming mice to study their the anti-drunk hangover effects and its mechanism, and the model was made by intragastric administration of 56 %vol liquor of Red Star Erguotou, China.The results showed that the middle dose (240 mg/kg) and high dose (400 mg/kg) of KGM could effectively prolong the climb time and Latency time of drunkenness, and could significantly shorten the drunken mice sleeping time and sobering time.The ethanol concentration of serum in the high and middle dose groups was significantly lower than that in the model group, and the contents of alcohol dehydrogenase (ADH), aldehyde dehydrogenase (ALDH) and cytochrome P450 (P450) in liver homogenate significantly increased in high dose group.The contents of malondialdehyde (MDA) in gastric mucosal tissues and serum in the middle and high dose groups significantly decreased, while the activities of superoxide dismutase (SOD), nitric oxide (NO) and prostaglandin E2 significantly increased.The anti-alcohol hangover mechanism of KGM might be as follows.On the one hand, alcohol absorption was inhibited by the KGM and the ethanol concentration in serum is reduced.On the other hand, the decrease of MDA content, and the increase of SOD activity, NO and PGE in gastric mucosa and serum decreased the damage of gastric mucosa, and increased the ADH, ALDH, P450.Thusand the alcohol metabolism was accelerated through alcohol dehydrogenase and ethanol oxidase system, then its anti-drunk hangover role was played.