Table 1.
Plants used for prevention and treatment of alcohol abuse in different folk medicine practices.
| Botanical name | Main phytochemical structure | Possible mechanism |
|---|---|---|
| Pueraria montana var. lobata (Willd.) Maesen & S.M.Almeida ex Sanjappa & Predeep (syn. Pueraria lobata (Lour.) Merr.) | Isoflavones derivatives (daidzin, puerarin) | 1. Reversible inhibition of mitochondrial ALDH-2 and increase of 5-hydroxyindole 3- acetaldehyde (5-HIAL) (Keung and Vallee, 1998a; Keung and Vallee, 1993b; Lu et al., 2009). 2. Alteration of BDZ receptors positioned on GABA-chloride channel complex (Shen et al., 1996; Keung and Vallee, 1998). 3. Alcohol-induced inhibition and disruption of hippocampus function leading to the suppression of c-fos protein (FOS) expression (Jang et al., 2003; Rezvani et al., 2003). |
| Salvia miltiorrhiza Bunge | Phenanthrenequinones compounds including cryptotanshinone, tanshinones I, II, and miltirone | 1. Militirone, low-affinity ligand for central GABAA-BDZ–binding site, thus acting as a partial agonist and implying an anxiolytic effect (Lee et al., 1991). 2. Miltirone partly inhibits upsurge in mRNA levels of the α 4 subunit of GABA that was persuaded through ethanol withdrawal in cultured hippocampal neurons (Mostallino et al., 2004; Zhu et al., 2017). 3. Tanshinone IIA improves alcoholic liver disease by decreasing lipopolysaccharide and Kupffer cell sensitization induced by alcohol (Yin et al., 2008). 4. Cryptotanshinone inhibits ALD through hindering fatty acid synthesis and hepatic cell death (Yin et al., 2009). |
| Hypericum perforatum L. | Phloroglucinol derivatives (adhyperforin, hyperforin), and anthraquinone derivatives (hypericin, pseudohypericin) | 1. Inhibits the uptake of serotonin and noradrenaline (aminergic transmitters) in the synaptic nerve endings (Butterweck et al., 1997; Kumar et al., 2006). 2. Increase in level of serotonin, dopamine, norepinephrine or through stimulation of opioid and sigma receptors in the CNS (Müller et al., 1997; Panocka et al., 2000). |
| Panax ginseng C.A.Mey. | Ginsenosides | 1. Increase of metabolism of alcohol and decreased blood alcohol levels (BALs) by enhancing ADH activity and plasma clearance (Lee et al., 1993). 2. Incite the microsomal ethanol-oxidizing system and ADH action and thereafter fasten the removal of acetaldehyde while shunting the excessive hydrogen into lipid biosynthesis (Abenavoli et al., 2009). |
| Tabernanthe iboga Baill. | Ibogaine | 1. Suppressive effect on alcohol intake by regulating several neural pathways particularly dopaminergic and serotonergic systems (Deecher et al., 1992; Sweetnam et al., 1995; Overstreet et al., 2003). 2. Interacts with k-opiate receptor and inhibits k- receptor mediated dopamine release in rats (Deecher et al., 1992; Reid et al., 1994). |
| Withania somnifera (L.) Dunal | Withanolide D and withaferin A | Blocks GABA receptors binding and up-surges chloride influx in absence of GABA (Gupta and Rana, 2008; Lu et al., 2009; Ruiu et al., 2013). |
| Macropiper methysticum (G.Forst.) Miq. (syn. Piper methysticum G.Forst.) | Kava lactones | 1. Binding to multiple locations in the brain and interaction with different neurotransmitters and significant inhibition of the uptake of noradrenaline, but not serotonin (Sällström Baum et al., 1998). 2. Also affects the concentration of dopamine and its metabolites that is/are in turn associated with altered behavioral response in rats (Sällström Baum et al., 1998). |
| Thunbergia laurifolia Lindl. | Iridoid glucosides of 8-epi-grandifloric acid and 3'-O-β-glucopyranosyl stilbericoside | 1. Increase of blood flow signals in amygdala, nucleus accumbens, frontal cortex, and caudate putamen (areas in the brain linked with addictive drug pathways) (Thongsaard et al., 2005). 2. Shares similarity with amphetamine in increasing potassium-triggered dopamine release from rat striatal slices, suggesting the potential efficacy for addictive drugs is dopamine-dependent (Thongsaard and Marsden, 2002). |
| Banisteriopsis caapi (Spruce ex Griseb.) Morton | Beta-carbolines, such as harmine, harmaline, and tetrahydroharmine (THH) | 1. Harmine and harmaline showed substantial inhibitory (in vitro) activity against MAO-A and -B in human brain and stimulate dopamine release (Samoylenko et al., 2010). 2. THH can also inhibit serotonin reuptake (Samoylenko et al., 2010). |
| Corydalis yanhusuo (Y.H.Chou &Chun C.Hsu) W.T.Wang ex Z.Y.Su & C.Y.Wu | Lev-tetrahydropalmatine (L-THP) | 1. L-THP inhibits oxycodone-induced hyperactivity (Liu et al., 2005). 2. Anti-addictive properties may be due to dopamine transmission antagonism. 3. Inhibits dopamine receptors D1 and D2 and acts upon the nigra-striatal neuronal pathways and inhibits pre- and post-synaptic receptors (Marcenac et al., 1986; Jin, 1987). 4. Prevents L-type Ca2+ channels inhibition; here it is notable that L-type Ca2+ channel inhibition is vital for the development of drug tolerance, sensitization, and dependence (Jin, 1987). |
| Lophophora williamsii (Lem. ex SalmDyck) J.M. Coult. | Mescaline (3,4,5-trimethoxy-β-phenylethylamine) | The mescaline molecule is structurally similar to serotonin and acts on the serotonin (5-HT2A) receptor. 5-HT2A receptors activation increases cortical glutamate levels apparently through a pre-synaptic receptor-mediated release from thalamic afferents (Nichols, 2004; Gibbons and Arunotayanun, 2013). |
| Hovenia dulcis Thunb. | Ampelopsin, hovenitins I, II, & III, laricetrin, myricetin, and gallocatechin | 1. Decrease of gastrointestinal absorption of alcohol and reducing of blood alcohol concentration (Xu et al., 2005). 2. Effective in enhancing ALDH activity than ADH activity, blocks lipid peroxidation, and eradicates unwarranted free radicals produced by alcohol (Yoshikawa et al., 1996b; Hase and Basnet, 1997; Xu et al., 2004). |
| Oenothera biennis L. | γ-linolenic acid (GLA) | 1. Excess alcohol consumption hinders the metabolism of GLA, which is a precursor of prostaglandins. As a result, prostaglandins E1 (PGE1) levels are reduced in alcohol addicts, often leading to depressive states that increase patients' inclination to drink. The need to drink is thus indirectly lowered by a reduction in the depression symptoms (Tomczyk et al., 2012). 2. Protects liver and kidney damage caused by alcohol intake by counteracting the enzyme inhibition (Glen et al., 1987; Abenavoli et al., 2009; Tomczyk et al., 2012) |