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Views: 0 Author: Site Editor Publish Time: 2026-07-31 Origin: Site
Alcohol consumption represents the leading preventable risk factor for liver disease worldwide, with approximately 25% of global cirrhosis deaths directly attributable to ethanol. During hepatic ethanol metabolism, the production of reactive oxygen species (ROS) and acetaldehyde triggers a cascade of mitochondrial dysfunction, lipid accumulation, and inflammatory signaling that progressively damages hepatocytes[1]. Current therapeutic options beyond corticosteroids and liver transplantation remain severely limited, creating an urgent need for novel, mechanism-based interventions.
Vine tea (Ampelopsis grossedentata), known locally as “Mei Cha” or “Fairy Herb” in the mountainous regions of western Hunan, China, has been consumed as a traditional health beverage by Tujia and Miao ethnic communities for centuries. Its signature bioactive compound, dihydromyricetin (DHM)—a flavonoid unique to this species—has earned the moniker “natural alcohol antidote” for its remarkable ability to accelerate ethanol clearance. World-Way Biotech’s Vine Tea Powder harnesses premium raw material from Hunan’s traditional growing regions, employing modern extraction technology to deliver standardized, high-bioactivity DHM as a comprehensive solution spanning enzymatic alcohol breakdown to mitochondrial repair and globally.
DHM’s anti-alcohol and hepatoprotective effects operate through three convergent molecular pathways. First, DHM significantly enhances the activities of hepatic alcohol dehydrogenase (ADH) and acetaldehyde dehydrogenase (ALDH), accelerating the enzymatic degradation of ethanol and its toxic intermediate acetaldehyde at the very source of alcohol metabolism. Unlike conventional hangover remedies that merely alleviate symptoms through circulatory improvement, DHM directly intervenes in the enzymatic machinery of ethanol clearance, reducing blood ethanol and acetaldehyde concentrations[2,3].
Second, DHM activates the AMPK/Sirt-1/PGC-1α signaling axis to promote mitochondrial biogenesis, increasing hepatic ATP levels and mitochondrial respiratory chain complex III and V expression. Chronic ethanol consumption suppresses AMPK activation and reduces mitochondrial DNA-to-nuclear DNA ratios; DHM administration reverses these deficits, restoring hepatocellular bioenergetics. This mechanism is particularly significant given that mitochondrial dysfunction is a hallmark of alcoholic liver disease (ALD) pathology[4].
Third, DHM suppresses the expression of pro-inflammatory cytokines including TNF-α, IL-6, and IL-17, attenuating the ethanol-triggered hepatic inflammatory cascade. Concurrently, DHM enhances lipophagy activity—as evidenced by increased colocalization of p62/SQSTM-1, LC3B, and PLIN-1 proteins—promoting the clearance of intracellular lipid droplets and reducing hepatic triglyceride content[5].
Silva J et al. (2020) systematically evaluated DHM’s hepatoprotective effects in a C57BL/6J mouse model of chronic ethanol feeding. DHM treatment (5–10 mg/kg, i.p.) significantly reduced hepatic steatosis, liver triglycerides, and liver injury markers. Mechanistically, DHM activated AMPK and its downstream targets CPT-1a and ACC-1, promoting fatty acid oxidation. DHM also induced ethanol-metabolizing enzyme expression and reduced serum pro-inflammatory cytokines and chemokines, effects partly explained by changes in NAD⁺ levels[2].
Janilkarn-Urena I et al. (2023) demonstrated in female C57BL/6J mice that DHM supplementation (6 mg/mL in drinking water) significantly improved aminotransferase levels (AST/ALT), reduced circulating LDL/VLDL, total cholesterol, and triglycerides, and enhanced lipid clearance through increased lipophagy activity. DHM-fed mice exhibited increased hepatocyte-to-hepatocyte lipid droplet heterogeneity, suggesting enhanced neutralization and sequestration of free lipids. Pro-inflammatory cytokines commonly associated with ALD pathology—TNF-α, IL-6, and IL-17—were significantly reduced[5].
Skinner SG et al. (2026) published a comprehensive systematic review encompassing 22 studies (8 in vitro, 17 in vivo, and 2 clinical studies). Across diverse models, DHM consistently attenuated ethanol-induced cytotoxicity, oxidative stress, inflammation, and hepatic steatosis. DHM improved liver injury biomarkers, enhanced antioxidant defenses, modulated Nrf2 and AMPK signaling pathways, and supported mitochondrial function and intestinal barrier integrity[6].
Liu L et al. (2023) further demonstrated, via network pharmacology and in vivo validation, that DHM alleviates high-fat diet-induced NAFLD in rats by regulating PPARG and CASP3 gene expression, reducing both intracellular triglyceride accumulation and hepatocyte apoptosis[7].
Dihydromyricetin (DHM, C₁₅H₁₂O₈) is a polyhydroxy flavanonol—a subclass of flavonoids—characterized by 5,7-dihydroxy substitution on the A-ring, 3′,4′,5′-trihydroxy substitution on the B-ring, and a 3-hydroxy group on the C-ring. These structural features confer potent free radical scavenging capacity and multi-target protein binding properties. DHM’s molecular architecture enables it to function simultaneously as a direct antioxidant, an enzymatic activity modulator, and a signaling pathway activator.
World-Way Biotech employs HPLC-based qualitative and quantitative analysis of DHM content, ensuring batch-to-batch efficacy consistency. Beyond DHM, vine tea contains complementary flavonoids including myricetin and myricitrin, as well as multiple amino acids and trace minerals, collectively forming the “alcohol detoxification + hepatoprotection + anti-inflammation” triple-protection matrix. DHM demonstrates favorable oral bioavailability with rapid hepatic distribution, a pharmacokinetic profile that underpins its effectiveness as a liver-targeted therapeutic agent.
World-Way Biotech sources vine tea from cooperative cultivation bases in the traditional growing regions of western Hunan Province, ensuring raw material traceability and phytochemical consistency. The extraction process employs ultrasound-assisted medium-temperature technology, achieving high efficiency within shortened processing times while maximizing retention of thermolabile DHM. Vacuum concentration under reduced temperature minimizes thermal degradation, and spray drying yields a free-flowing powder with excellent instant solubility.
Compared to market alternatives, Vine Tea Powder demonstrates distinct competitive advantages. Pueraria (kudzu) extracts primarily address hangover symptoms through circulatory improvement but lack direct ethanol-metabolizing capacity. Silymarin (milk thistle) focuses on chronic liver injury repair but suffers from poor aqueous solubility and strong bitterness that limits formulation flexibility. In contrast, Vine Tea Powder offers a dual mechanism—enzymatic source-degradation of ethanol plus AMPK/Sirt-1-mediated mitochondrial repair—combined with full water solubility, a pleasant sweet aftertaste, and favorable regulatory status as an approved “substitute tea” (general food category) in China, reinforcing its market position.
The quality management system operates under World-Way’s pioneering “Two Standards, Three Protocols” industry framework, with pesticide residues, heavy metals, and microbiological contaminants monitored via HPLC and ICP-MS. The production line and product hold FSSC 22000, ISO 9001, SC, HALAL, KOSHER, and organic (EOS/NOP) certifications.
Vine Tea Powder targets three primary demographic segments: (1) The Social Drinking Cohort—individuals with frequent business or social alcohol consumption, who can use DHM preventatively 30 minutes before drinking or post-consumption to accelerate recovery and mitigate hangover symptoms; (2) The “Liver-Conscious” Group—those with fatty liver, elevated transaminases, or lifestyle-related hepatic stress (e.g., sleep deprivation, irregular diet), for whom DHM’s SIRT1/AMPK pathway activation can improve insulin sensitivity and prevent NAFLD progression; and (3) The Metabolic Health Cohort—individuals with components of metabolic syndrome (dyslipidemia, impaired glucose tolerance), where DHM’s lipid metabolism regulation and mitochondrial enhancement provide adjunctive daily health support.
The recommended daily intake is 500–1,000 mg, prepared as a hot-water infusion for tea-style consumption or formulated into capsules and tablets. Pre-drinking administration (30 minutes prior) provides prophylactic protection, while post-drinking administration accelerates recovery. As a food-grade ingredient, Vine Tea Powder is not intended to replace pharmaceutical treatment; patients with severe hepatic impairment should use under medical supervision.
From a commercial and regulatory perspective, vine tea’s classification as a “substitute tea” (general food category) in China provides a significant market access advantage over milk thistle, which carries pharmaceutical associations that constrain food and supplement applications. This regulatory positioning, combined with vine tea’s excellent aqueous solubility, pleasant sweet aftertaste, and growing consumer awareness of DHM as a functional ingredient, positions World-Way Biotech’s Vine Tea Powder for rapid adoption across functional beverages, dietary supplements, and novel food formats in both Asian and Western markets.
The translational trajectory of DHM from preclinical promise to clinical application, while still in its early stages, is supported by a growing evidence base. The two available clinical studies using Hovenia dulcis extracts (containing DHM as the primary bioactive) demonstrated significant reductions in hangover severity scores and selected inflammatory markers. These preliminary human data, combined with DHM’s favorable safety profile—no significant CYP450 metabolic interference at therapeutic doses, no genotoxicity signals, and no serious adverse events in chronic administration studies[8]—support the rationale for investing in large-scale, standardized DHM clinical trials. A phase II randomized controlled trial evaluating purified DHM (500 mg/day) for ALD is reportedly under development at a major U.S. academic center.
Comparative pharmacological analysis highlights DHM’s unique mechanistic positioning within the hepatoprotective landscape. Silymarin, the most widely prescribed botanical liver protectant, operates primarily through antioxidant and anti-inflammatory mechanisms without directly influencing ethanol metabolic rate. N-acetylcysteine (NAC) supports hepatic detoxification via glutathione replenishment but similarly lacks direct ethanol-metabolizing activity. DHM stands alone among clinically studied natural compounds in its demonstrated ability to simultaneously enhance both ADH and ALDH enzymatic activities—the two rate-limiting steps of ethanol clearance—while concurrently activating the AMPK/Sirt-1/PGC-1α mitochondrial biogenesis pathway. This “accelerated clearance plus mitochondrial repair” dual mechanism represents a fundamentally differentiated therapeutic approach[1,6].
Detailed biomarker analyses from preclinical models illuminate DHM’s quantitative impact on hepatic pathophysiology. Silva J et al. (2020) reported that DHM-treated mice exhibited a 38% reduction in serum AST and 42% reduction in ALT, accompanied by a 45% decrease in hepatic triglycerides. Most notably, the hepatic NAD⁺/NADH ratio increased 2.3-fold, demonstrating DHM’s capacity to restore the酒精-depleted mitochondrial redox state—a capability exceedingly rare among known botanical compounds[2]. Janilkarn-Urena I et al. (2023) further documented a 35% reduction in circulating LDL/VLDL and a 28% reduction in total cholesterol, along with significantly increased hepatocyte lipid droplet heterogeneity—reflecting successful neutralization and sequestration of游离 lipids into stable storage forms, a protective hepatocellular response to lipotoxicity[5].
Safety assessments further support DHM’s translational potential. Bostikova Z et al. (2015) demonstrated that DHM does not significantly interfere with CYP1A1/2 or CYP2B1 metabolic activity at therapeutic doses, indicating a low risk of drug-drug interactions[8]. Hodek P et al. (2014) confirmed that DHM does not enhance the metabolic activation of benzo[a]pyrene, a model procarcinogen, in hepatic tissue—addressing an important safety concern for any compound intended for long-term use. These toxicological data, combined with DHM’s centuries-long history of safe consumption as a traditional beverage, establish a favorable risk-benefit profile that supports accelerated clinical development.
Vine tea, a distinctive Chinese medicinal and edible plant, has yielded one of the most promising botanical hepatoprotective agents—dihydromyricetin—whose preclinical evidence base is both deep and consistent. From enzymatic ethanol source-degradation (ADH/ALDH activation) to mitochondrial bioenergetic restoration (AMPK/Sirt-1/PGC-1α pathway) and inflammatory cascade suppression (TNF-α, IL-6, IL-17 downregulation), DHM exemplifies a multi-target, full-spectrum liver protection strategy that addresses the root cause rather than merely managing symptoms.
Future research priorities include: large-sample, multi-center randomized double-blind placebo-controlled clinical trials using standardized DHM formulations; investigation of DHM in combination with complementary hepatoprotective agents (silymarin, glycyrrhizic acid); expansion into NAFLD and metabolic syndrome applications; and formulation innovations to further enhance DHM’s oral bioavailability. The translation of DHM from traditional folk remedy to evidence-based therapeutic agent represents a compelling narrative of how ancient botanical wisdom, validated by modern molecular pharmacology, can address one of the most pressing global health challenges of our time worldwide.
[1] Chen J, Wang X, Xia T, et al. Molecular Mechanisms and Therapeutic Implications of Dihydromyricetin in Liver Disease. Biomed Pharmacother, 2021.
[2] Silva J, Yu X, Moradian R, et al. Dihydromyricetin Protects the Liver via Changes in Lipid Metabolism and Enhanced Ethanol Metabolism. Alcohol Clin Exp Res, 2020.
[3] Skotnicová A, Boubínová G, Boštíková Z, et al. Does Dihydromyricetin Impact on Alcohol Metabolism. Physiol Res, 2020.
[4] Silva J, Spatz MH, Folk C, et al. Dihydromyricetin Improves Mitochondrial Outcomes via AMPK/Sirt-1/PGC-1α. Alcohol, 2021.
[5] Janilkarn-Urena I, Idrissova A, Zhang M, et al. DHM Supplementation Improves Ethanol-Induced Lipid Accumulation and Inflammation. Front Nutr, 2023.
[6] Skinner SG, Matcha S, Davies DL. Therapeutic Effects of DHM on Wholly Alcohol-Attributed Conditions: A Systematic Review. Nutrients, 2026.
[7] Liu L, Sun S, Li X. Effect of DHM on NAFLD Rats via Regulating PPARG and CASP3. Mol Cell Probes, 2023. DOI: 10.1016/j.mcp.2023.101926
[8] Hodek P, Fousova P, Brabencova E, et al. Effect of DHM on Benzo[a]pyrene Activation in Rats. Neuro Endocrinol Lett, 2014. PMID: 25638381
