IngredientsVine tea (Ampelopsis grossedentata Hand.-Mazz. W.T.Wang) is also known by the common names "Teng Cha," "Tocha," "Rattan tea," "Duan Wu Cha," "Mao Yan Mei," and "Moyeam." Botanically, it belongs to the grape family (Vitaceae) and the snake grape genus (Ampelopsis). The species also carries the accepted synonym Nekemias grossedentata (Hand.-Mazz.) J.Wen and Z.L.Nie, used in some contemporary literature.
Taxonomically belonging to the genus Ampelopsis in the Vitaceae family, its wild resources are mainly distributed in mountainous areas of southern China such as Hubei, Hunan, Guangdong, Guangxi, and Jiangxi, and regions with large ethnic minority populations. It grows in high mountains at altitudes of 800 to 1500 m and is mostly cultivated in Zhangjiajie, a mountainous region in central China's Hunan province.
It is a species of perennial woody vine, mainly distributed in southern China. Originally a vine plant that climbs scattered on wastelands, roadsides, and thickets, it becomes semi-erect after artificial cultivation to facilitate picking of young stems and leaves.
The dried stems, leaves, and shoot tips, known as "vine tea," are consumed as a health beverage and traditional remedy. The substitute tea made from its young stems and leaves has different names among different regions and ethnic groups due to variations in picking time, processing methods, customs, and product appearance, such as Duanwu tea, Meicha, Zhangjiajie Meicha, Maoyan Meicha, sweet tea, Ganchamei, longevity vine, Bangbang tea, and others. When made into tea cakes, it is also called white tea cake.
Historically, vine tea bore the name "mold tea" because after processing, the leaves develop a natural white frost-like coating, giving them a mold-like appearance. Today, A. grossedentata is commonly used in dietary supplement forms such as teas, beverages, and lozenges. Standardized extracts, capsules containing purified dihydromyricetin, and fermented broth preparations also appear in the scientific literature.
Vine tea boasts a recorded consumption history exceeding 1200 years, predominantly utilized by ethnic groups in southwest China, and traditionally celebrated for its multifaceted therapeutic attributes including alleviating heat and removing toxins, exhibiting anti-inflammatory properties, soothing sore throats, lowering blood pressure, and fortifying bones and muscles.
Vine tea has been consumed in China for thousands of years and is considered a therapeutic tea or herbal tea in the Tujia, Yao, and Hakka regions of China for anti-inflammatory purposes and treatment of sore throat. The Yao minority of Guangxi and Hunan made vine tea from its stems and leaves to alleviate cold and fever, sore throat, jaundice, and hepatitis, as well as prevent and treat nephritis, halitosis, and polyphagia.
It is widely acknowledged that vine tea was used as a medicinal herb in traditional Chinese medicine to clear away heat, promote diuresis, and support blood circulation, and that people in China used vine tea to treat hypertension and diseases such as heart disease and chronic pharyngitis for hundreds of years.
In classical Chinese medicine, A. grossedentata was regarded as having the effects of "regulating Zhong, replenishing Qi and circulating blood and Qi," as recorded in the Compendium of Materia Medica. As a medicinal plant, A. grossedentata has been used for centuries for various therapeutic purposes to prevent and treat symptoms such as colds, fevers, sore throats, and toothaches.
Dihydromyricetin is thought to be the active ingredient of several traditional Japanese, Chinese, and Korean medicines used to treat fever, parasite infections, liver diseases, and hangovers. DHM has traditionally been used in Asian medicine to naturally counteract ethanol intoxication and prevent hangovers.
Approximately 57 chemical components of A. grossedentata have been identified, including flavonoids, phenols, steroids and terpenoids, volatile components, and other chemical compounds. Current research has identified the primary phytochemical constituents as flavonoids, terpenoids, and polyphenolic compounds. It is rich in bioactive compounds, including flavonoids, polysaccharides, alkaloids, and polyphenols.
With its total flavonoid content reaching 35–45%, A. grossedentata is the plant with the highest known concentration of flavonoids, providing it significant commercial potential and vast market opportunities. The plant has accordingly been referred to as the "king of flavonoids" in the Chinese scientific literature.
More than 20 different flavonoids have been isolated and identified from vine tea. Five major flavonoids detected and identified by LC–MS include quercetin, dihydromyricetin, iso-dihydromyricetin, myricetin-3-O-rhamnoside, and myricetin. Flavonoids in vine tea mainly include dihydromyricetin (DMY), myricetin, myricitrin, and myricetin-3-β-D-galactopyranoside.
Dihydromyricetin (3,5,7,3′,4′,5′-hexahydroxy-2,3-dihydroflavonol, DHM), also known as ampelopsin, has a content in A. grossedentata ranging from 30% to 40% of dry weight, which is considered to have the highest flavonoid content in natural plants. It is a naturally occurring dihydroflavonol compound primarily derived from A. grossedentata, where it accounts for about 35% of total flavonoids and is the most abundant flavonoid monomer in the plant.
DHM is also found, in smaller amounts, in other plant species. These include Hovenia dulcis (Japanese raisin tree) and some Pinus and Cedrus species.
A major disadvantage associated with DMY is its chemical instability and poor bioavailability caused by the combined effects of its low solubility and poor membrane permeability, which limits its practical use in the food and pharmaceutical fields. The phenol hydroxyl groups of DHM make it chemically unstable; oxidation is reported as the main cause of degradation, and avoiding metal ions, high temperature, and alkaline conditions during processing and storage is important. Preclinical studies are underway to try to develop more stable, bioavailable formulations of DHM with pharmacokinetic properties better suited for therapeutic use.
DHM has been found to significantly activate the Keap-1/Nrf2/HO-1 pathway, enhancing antioxidant defense mechanisms and reducing oxidative damage. DMY also prevented oxidative stress in LDL receptor–deficient mice on a high-fat diet, possibly related to normalizing antioxidant enzymes' activities to suppress reactive oxygen species generation and NOX2 expression.
DHM inhibits the NF-κB and caspase-3 pathways, leading to reductions in inflammation and apoptosis. DHM possesses pharmacological effects including anti-inflammatory actions involving inhibition of NLRP-3, NF-κB, cytokines, and neuroinflammation.
The collective effects of DHM include increasing antioxidant enzymes and inducing AMP-activated protein kinase (AMPK) metabolic signaling, resulting in reduced steatosis and inflammation. DHM exerts anti-insulin resistance effects by inducing autophagy via activation of the AMPK-PGC-1α-Sirt3 signaling pathway. DHM exerts hypoglycemic effects through multi-target regulation of the AMPK/AKT/GSK-3β pathway, which includes enhancing insulin sensitivity and inhibiting hepatic glucose production.
DHM exhibits inhibitory effects on the activities of α-amylase and α-glucosidase, which aids in reducing the hydrolysis of carbohydrates in the diet, thereby lowering postprandial blood glucose levels.
Evidence suggests that the mechanism of the anti-ethanol properties of DHM may be linked to specific GABAA receptor molecular interactions at the benzodiazepine binding site; electrophysiology studies indicate DHM acts as a GABAAR positive modulator and inhibitor of ethanol-induced GABAAR potentiation, and both ex vivo and in vivo anti-ethanol effects of DHM were antagonized dose-dependently by the addition of flumazenil, a benzodiazepine antagonist.
Preclinical studies have focused on the potential beneficial effects of DHM on glucose metabolism regulation, lipid metabolism regulation, neuroprotection, and anti-tumor effects, and DMY may play a role in cardiovascular disease by resisting oxidative stress and participating in the regulation of inflammation. DHM has been shown to increase orphan nuclear receptor TR3 expression in smooth muscle cells (SMCs) and carotid artery, promoting SMC differentiation while inhibiting SMC proliferation and migration.
Non-alcoholic Fatty Liver Disease (NAFLD) — Human Clinical Evidence: In a double-blind clinical trial, sixty adult NAFLD patients were randomly assigned to receive either two dihydromyricetin or two placebo capsules (150 mg) twice daily for three months. Serum levels of alanine aminotransferase, aspartate aminotransferase, γ-glutamyl transpeptidase, glucose, LDL-cholesterol, and apolipoprotein B, and the homeostasis model assessment of insulin resistance (HOMA-IR) index were significantly decreased in the dihydromyricetin group compared with the placebo group; additionally, tumor necrosis factor-alpha, cytokeratin-18 fragment, and fibroblast growth factor 21 were decreased, whereas adiponectin was increased. The authors concluded that DHM supplementation improves glucose and lipid metabolism as well as various biochemical parameters in NAFLD, with effects likely attributable to improved insulin resistance and reductions in inflammatory markers. The authors noted this constituted the first randomized, double-blind clinical pilot study on DHM supplementation in NAFLD. As a pilot trial of 60 patients, the evidence base remains limited and requires confirmation by larger, independent trials.
Alcoholic Liver Disease — Preclinical Evidence: Studies have shown that AGE offers significant protection against liver diseases including alcoholic liver disease (ALD), non-alcoholic fatty liver disease (NAFLD), and acute liver injury, based on preclinical models. The collective effects of DHM — increasing antioxidant enzymes and inducing AMPK metabolic signaling — result in reduced steatosis and inflammation in animal models. Human clinical data for alcoholic liver disease specifically remain lacking as of available literature.
Ischemia/Reperfusion Injury — Preclinical Evidence: In animal studies, DHM markedly decreased serum aminotransferase activity and inhibited liver ischemia/reperfusion–stimulated apoptosis; DHM exerted hepatoprotective effects by upregulating mRNA levels of essential autophagy-related genes including ATG5, ATG12, BECN1, and LC3. All evidence for this indication is preclinical.
Liver Safety Profile: Dihydromyricetin preparations have not been linked to instances of serum enzyme elevations or clinically apparent liver injury with jaundice.
Human Clinical Evidence: Compared with placebo, levels of fasting blood glucose, glycated albumin, bladder C, and RBP-4 were significantly decreased in the vine tea group in a clinical study. However, the limitations of this first clinical research include a small sample size. Ran et al. reported that Ampelopsis grossedentata is helpful in ameliorating glucose levels in patients with type 2 diabetes. A randomized controlled trial showed that dihydromyricetin improved glucose and lipid metabolism and exerted anti-inflammatory effects in patients with non-alcoholic fatty liver disease.
Animal Evidence: Vine tea regulates glucose and lipid metabolism, increases insulin sensitivity, and improves hepatic lipid accumulation in high-fat diet–induced rats, with mechanisms related to the improvement of energy-related metabolism and the decrease of lipid accumulation. In db/db mice, vine tea dihydromyricetin extract (VDMY) significantly reduced fasting blood glucose, total cholesterol, triglycerides, and LDL-C, while increasing HDL-C levels. In a study using 10-week-old db/db mice, DHM was administered at 1.0 g and 0.5 g/kg body weight simultaneously with a high-fat diet for 8 weeks, with metformin (50 mg/kg BW) used as a positive reference drug.
Evidence Characterization: For metabolic syndrome and glycemic control, there are a small number of human clinical studies with encouraging but preliminary results. The preponderance of evidence is animal-based and cannot be extrapolated directly to humans. According to ClinicalTrials.gov, a Phase 2 clinical trial (NCT03606694) was registered to test DHM against metformin for its effects on glycemic control, insulin sensitivity, and insulin secretion in type 2 diabetes mellitus.
Preclinical Evidence: In rats given intraperitoneal injections of DHM, there was decreased voluntary intake of alcohol, less evidence of alcohol central nervous system effects, and fewer signs of subsequent alcohol withdrawal; these effects were attributed to DHM's effects on GABA signaling. Preclinical studies in rats demonstrated DHM to substantially reduce ethanol-induced loss of righting reflex, subsequent withdrawal symptoms, ethanol-induced GABAAR plasticity, and prevent physiological symptoms of fetal alcohol syndrome.
Human Evidence: DHM is sold as a supplement and is commonly marketed as a treatment for hangovers due to its ability to reduce blood alcohol levels and projected hepatoprotective properties. Direct, well-powered human clinical trials investigating the effect of A. grossedentata-derived DHM specifically on hangover severity remain limited in the published literature, though such trials have been registered.
Evidence Characterization: The anti-alcohol and hangover evidence for DHM is compelling at the preclinical level and the mechanistic basis (GABAergic modulation) is well characterized, but robust human clinical trials focused specifically on A. grossedentata-derived DHM are not yet established in the published record. Evidence should be considered preliminary.
Preclinical Evidence: Preclinical research has summarized applications of DHM in cardiovascular diseases including atherosclerosis, myocardial infarction, myocardial hypertrophy, and diabetic cardiomyopathy. DHM has been demonstrated to enhance cardiac function in streptozotocin-induced diabetic mice, ameliorating myocardial hypertrophy, fibrosis, and injury while suppressing oxidative stress, inflammation, and cell death through the activation of SIRT3. DHM also exhibits cardioprotective effects by mitigating cardiac toxicity; research demonstrates that DHM inhibits NLRP3 inflammasome activation through the SIRT1 pathway, effectively preventing doxorubicin-induced cardiac toxicity.
Studies determined that ligation-induced carotid artery neointimal formation could be significantly attenuated by DHM treatment in animal models.
Evidence Characterization: All cardiovascular evidence for vine tea and DHM is preclinical (in vitro and animal models). No human cardiovascular clinical trials were identified in the available literature.
Preclinical Evidence: Studies have shown that DHM is capable of safeguarding the brain via activation of the Nrf2 and Prx2 signaling pathways, resulting in a notable decline in neuronal oxidative damage and apoptosis after subarachnoid hemorrhage; DHM also diminishes ferroptosis in brain tissue, thereby alleviating cerebral hemorrhages. DHM has a positive effect on Parkinson's disease (PD); in a PD-like mouse model, DHM alleviated motor dysfunction and prevented the loss of dopaminergic neurons. Studies have revealed that DHM ameliorates anxiety behavior in a chronic social isolation mouse model by regulating mitochondrial function, reducing oxidative stress, restoring normal autophagy, and increasing brain-derived neurotrophic factor (BDNF).
DHM pre-treatment (10 mg/kg/day) decreased the time of initiating movement and passing across the beam, hang time, and time to find the platform, suggesting that motor behavior, learning, and memory ability were improved by DHM in 3-nitropropionic acid–induced rats.
Evidence Characterization: All neuroprotective evidence is preclinical. No human clinical trials for neurological indications were identified in the available literature.
Preclinical Evidence: DHM inhibits the progression of cancers such as lung cancer, hepatocellular cancer, breast cancer, melanoma, and malignant reproductive system cancers through multiple mechanisms including antiangiogenesis, antiproliferation, apoptosis, and inhibition of invasion and migration; DHM also activates autophagy at different levels, exerting a dual-regulatory effect on cancers. Mechanistically, DHM can regulate mTOR, noncoding RNA-mediated signaling, the PI3K/Akt pathway, NF-κB, p53, and endoplasmic reticulum stress–driven signaling.
Evidence Characterization: Anticancer evidence for DHM is entirely in vitro and in vivo (animal) based. No human clinical trials for oncology indications were identified. This area is considered early-stage and investigational.
In addition to anti-tumor activities, DHM also has antiviral and antibacterial activities demonstrated in laboratory studies. Numerous studies have reported antimicrobial activity as part of diverse pharmacological activities, though these derive primarily from in vitro experiments.
Evidence Characterization: Antimicrobial evidence is in vitro only. No clinical trials were identified for infectious disease indications.
Vine tea extract exhibits significant anti-fatigue effects, with mechanisms intricately linked to the modulation of the AMPK and FoxO pathways; crucially, no caffeine or other addictive substances with known side effects were detected in vine tea extract. The evidence for anti-fatigue effects is derived from animal models and in vitro studies; human clinical confirmation is lacking.
Downregulation of the ratio of Firmicutes and Bacteroidetes in the human gastrointestinal tract has been observed to alleviate metabolic disorders; the ratio is upregulated in obese patients, and levels of glucagon-like peptide 1 can be increased with the decrease of this ratio in insulin-resistant mice; these results suggest that vine tea and its extracts can interfere with metabolic syndrome by regulating the abundance and composition of gut microbes. Evidence for this mechanism in humans is largely indirect and inferred from animal data.
Vine tea and its principal isolate DHM are used in several forms, and dosages reported across studies vary considerably. The following dosages are drawn directly from the scientific literature:
No clinically validated therapeutic dose has been established for any indication. The functional food dosage of 3 g/day of whole vine tea is reported in animal-based metabolic research; dosages used in human trials are limited to the single NAFLD pilot RCT at 600 mg DHM daily.
Vine tea exhibits a wide range of significant bioactivities including anti-oxidant, anti-inflammatory, anti-tumor, antidiabetic, neuroprotective, and other activities, and is reported to show no toxicity in available studies. DHM is recognized for its high biosafety, making it a promising subject for further research.
Wistar rats orally gavaged with dihydromyricetin of purity more than 95% at 5.0 g/kg showed no abnormalities in sensory performance, behavioral performance, or animal dissection during a 14-day observation period, thus demonstrating that dihydromyricetin has no obvious toxic and side effects at this dose. A safety toxicological evaluation conducted by the Hunan Provincial Center for Disease Control and Prevention found that the acute oral toxicity test of A. grossedentata in mice was non-toxic, and three genotoxicity tests (Ames test, mouse bone marrow cell micronucleus test, and mouse sperm deformity test) were negative.
No caffeine or other addictive substances with known side effects were detected in vine tea extract. This distinguishes vine tea from conventional teas derived from Camellia sinensis.
A systematic compilation of all publications on the hepatotoxicity of specific herbal products identified 185 publications on 60 different herbs, herbal drugs, and supplements but does not list or mention DHM, consistent with its absence from known hepatotoxic agents. Dihydromyricetin preparations have not been linked to instances of serum enzyme elevations or clinically apparent liver injury with jaundice.
Despite its great development potential, DHM has problems in pharmaceutical applications such as low solubility, permeability, and stability. Avoiding metal ions, high temperature, and alkaline conditions during processing and storage is important to minimize degradation.
Given its mechanism of action as a GABAA receptor modulator, both ex vivo and in vivo anti-ethanol effects of DHM were antagonized dose-dependently by the addition of flumazenil, a benzodiazepine antagonist, suggesting a potential for pharmacodynamic interactions with benzodiazepines and related central nervous system depressants or reversal agents, though this has not been studied clinically. Additionally, given documented effects on glycemic enzymes (α-glucosidase inhibition) and the AMPK pathway, additive or synergistic effects with antidiabetic medications are theoretically possible but have not been characterized in human studies.
No clinically validated therapeutic dose has been established for any indication. Extensive research has been carried out on DHM's physicochemical properties and dosage forms to produce improved preparations, but bioavailability challenges persist. The majority of pharmacological evidence is derived from animal and cell-culture experiments, and translation to human therapeutic contexts has been only partially begun.
Health conditions that Vine tea may help support.
Body systems that Vine tea may help support.
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