二氢杨梅素

二氢杨梅素（DMY,Dihydromyricetin）

二氢杨梅素，是葡萄科蛇葡萄属的一种野生木质藤本植物提取物，其中主要活性成分为黄酮类化合物，此类物质具有清除自由基、抗氧化、抗血栓、抗肿瘤、消炎等多种奇特功效；而二氢杨梅素是较为特殊的一种黄酮类化合物，除具有黄酮类化合物的一般特性外，还具有解除醇中毒、预防酒精肝、脂肪肝、抑制肝细胞恶化、降低肝癌的发病率等作用。是保肝护肝，解酒醒酒的良品。

二氢杨梅素，是藤茶的主要活性成分之一具有多种生物学功能。又名双氢杨梅树皮素、福建茶素、白蔽素、二氢杨梅黄酮、蛇葡萄素等。

主要功能：

藤茶提取物具有多种功效：

1）清除自由基、抗氧化的作用：藤茶提取物能有效降低小鼠体内脂质过氧化水平，防止体内抗氧化酶受自由基的诱导的氧化损伤，显著增强机体抗氧化能力；

2）抗菌作用：藤茶提取物对金色葡萄球菌、枯草杆菌有很强的抑制效果，对黄曲霉、黑曲霉、青霉和交链霉均有不同程度的抑制效果。二氢杨梅素对金葡萄、耐药金葡萄和绿脓杆菌都有不同的抑制效果。

3）保肝作用：二氢杨梅素能明显抑制血清中丙氨酸转氨酶（ALT）和天冬氨酶转氨酶（AST）的活性升高及降低血清总胆红素，有明显的降酶退黄的作用。藤茶提取物能抑制大鼠肝纤维化的形成。

4）降血脂、降血糖的作用：二氢杨梅素能降低小鼠血脂，增强机体抗氧化能力，减轻高脂对肝细胞的损害。同时对高血糖小鼠有明显的降糖效果。

5）抗炎、镇疼效果：藤茶提取物能明显抑制二甲苯致小鼠耳廓肿胀，抑制乙酸诱发小鼠扭体反应。

6）抗肿瘤作用：藤茶提取物对部分癌细胞的增殖有明显的抑制作用。

Dihydromyricetin As a Novel Anti-Alcohol Intoxication Medication

1.Yi Shen1,

2. A. Kerstin Lindemeyer1,

3.Claudia Gonzalez1,

4.Xuesi M. Shao2,

5.Igor Spigelman3,

6.Richard W. Olsen1, and

7.Jing Liang1

1.1Departments of Molecular and Medical Pharmacology and

2.2Neurobiology, David Geffen School of Medicine, and

3.3Division of Oral Biology and Medicine, School of Dentistry, University of California,

Los Angeles, California 90095

1.Author contributions: X.M.S., I.S., R.W.O., and J.L. designed research; Y.S., A.K.L., C.G.,

and J.L. performed research; Y.S., A.K.L., C.G., X.M.S., and J.L. analyzed data; Y.S., X.M.S., I.S., R.W.O., and J.L. wrote the paper.

Abstract

Alcohol use disorders (AUDs) constitute the most common form of substance abuse. The development of AUDs involves repeated alcohol use leading to tolerance, alcohol withdrawal syndrome, and physical and psychological dependence, with loss of ability to control excessive drinking. Currently there is no effective therapeutic agent for AUDs without major side effects.

Dihydromyricetin (DHM; 1 mg/kg, i.p. injection), a flavonoid component of herbal medicines, counteracted acute alcohol (EtOH) intoxication, and also withdrawal signs in rats including tolerance, increased anxiety, and seizure susceptibility; DHM greatly reduced EtOH consumption in an intermittent voluntary EtOH intake paradigm in rats. GABA A receptors (GABA A Rs) are major targets of acute and chronic EtOH actions on the brain. At the cellular levels, DHM (1 μm) antagonized both acute EtOH-induced potentiation of GABA A Rs and EtOH exposure/withdrawal-induced GABA A R plasticity, including alterations in responsiveness of extrasynaptic and postsynaptic GABA A Rs to acute EtOH and, most importantly, increases in GABA A R α4 subunit expression in hippocampus and cultured neurons. DHM anti-alcohol effects on both behavior and CNS neurons were antagonized by flumazenil (10 mg/kg in vivo; 10 μm in vitro), the benzodiazepine (BZ) antagonist. DHM competitively inhibited BZ-site [3H]flunitrazepam binding (IC50, 4.36 μm), suggesting DHM interaction with EtOH involves the BZ sites on GABA A Rs. In summary, we determined DHM anti-alcoholic effects on animal models and determined a major molecular target and cellular mechanism of DHM for counteracting alcohol intoxication and dependence. We demonstrated pharmacological properties of DHM consistent with those expected to underlie successful medical treatment of AUDs; therefore DHM is a therapeutic candidate.