Dihydroquercetin, a member of the flavonol family, has garnered significant attention in the scientific and health fields. Its molecular formula is C₁₅H₁₂O₇, with a molecular weight of 304.25. Structurally, its molecular framework is derived from 2-phenylchromone, uniquely featuring five phenolic hydroxyl groups. These phenolic hydroxyl groups are not merely simple structural components; they play a crucial role in dihydroquercetin’s antioxidant activity, forming the core structural basis for its powerful antioxidant capacity. In complex biochemical reactions, the phenolic hydroxyl groups of dihydroquercetin act like highly trained “free radical hunters,” precisely capturing harmful free radicals. Whether it’s the highly oxidizing hydroxyl radical that attacks various intracellular biomolecules, or the superoxide anion that participates in numerous redox reactions in the body and can trigger oxidative stress in excess, neither can escape the “hunt” of dihydroquercetin. It provides hydrogen atoms to combine with free radicals, transforming them into relatively stable substances, thereby blocking the chain reaction initiated by free radicals and preventing further oxidative damage to cells.
Compared to vitamins C and E, which are familiar to us in daily life, dihydroquercetin’s antioxidant capacity is outstanding. Vitamins C and E have wide applications and high recognition in the field of antioxidants; they can scavenge free radicals to a certain extent and protect cell health. However, the antioxidant activity of dihydroquercetin far exceeds that of these two vitamins. Experimental data shows that, under the same conditions, dihydroquercetin’s efficiency in scavenging free radicals is several times or even dozens of times that of vitamin C, and it also has a significant advantage over vitamin E.
In addition to its powerful antioxidant activity, dihydroquercetin also possesses excellent stability. When exposed to common environmental factors such as light and high temperatures, the activity of many antioxidants is affected to varying degrees, and they may even lose some or all of their antioxidant capacity. However, dihydroquercetin exhibits remarkable stability. It maintains its molecular structure integrity under light exposure, continuing its antioxidant effects. Even at high temperatures, it does not easily decompose or undergo structural changes, effectively scavenging free radicals and providing stable and long-lasting protection for cells. This stability gives dihydroquercetin a significant advantage in various applications, whether as a food additive to extend shelf life or in skincare products to protect against UV damage. Therefore, dihydroquercetin is hailed as a rare “full-spectrum antioxidant” in nature, capable of comprehensively protecting organisms from free radical damage.
Natural Sources and Enrichment Pathways
Dihydroquercetin is widely distributed in nature, found in various plants, providing abundant sources for this natural treasure.
Larch and Douglas fir are important sources of dihydroquercetin. Especially larch trees growing in the Russian high-altitude region have high-purity dihydroquercetin extracts, with contents reaching 2-3%. The unique geographical environment and climate of the Russian high-altitude region create a special ecological environment for larch growth, allowing them to accumulate abundant dihydroquercetin during their growth. Extracting dihydroquercetin from these larch roots requires a series of complex and meticulous processes. First, larch roots are selected from trees of suitable age and healthy growth. Then, scientific extraction methods are used to separate dihydroquercetin from the plant tissue without damaging its structure and activity. This process requires not only advanced technology and equipment but also skilled technicians to ensure the quality and purity of the extract.
In our daily diet, common foods such as onions, apples, and grapes also contain dihydroquercetin. Although the content of dihydroquercetin in these foods is relatively low, the body can still obtain a certain amount of dihydroquercetin through daily consumption. For example, onions contain a variety of nutrients, including dihydroquercetin. When we eat onions, we ingest dihydroquercetin. Although the amount ingested each time may be small, long-term consumption can have a positive effect on health. Similarly, apples and grapes are also common fruits in our lives. They are not only delicious but also rich in various vitamins, minerals, and bioactive components, among which dihydroquercetin is one of the components with important health benefits.
To improve the bioavailability of dihydroquercetin and enable the body to better absorb and utilize this nutrient, scientists have conducted extensive research. One effective method is to combine dihydroquercetin with starch, such as adding dihydroquercetin during the cooking process of rice. Rice is one of the staple foods in people’s daily diet and is rich in starch. When dihydroquercetin combines with starch, starch acts as a carrier, helping dihydroquercetin pass more effectively through the human digestive system, reducing degradation and loss in the gastrointestinal tract, and thus improving its absorption efficiency in the body. This combination method is not only simple and easy to implement, but also makes full use of daily eating habits, allowing people to better absorb the nutrients of dihydroquercetin while enjoying food, making it a natural and ideal way to supplement the diet.
Multi-dimensional Health Empowerment: Core Efficacy Beyond Traditional Antioxidants
Multi-dimensional Health Empowerment: Core Efficacy Beyond Traditional Antioxidants(I) Antioxidant Defense: A Long-Lasting Shield for Cellular Anti-Aging
Dihydroquercetin can be considered an “antioxidant guardian” at the cellular level. Through its unique mechanism of action, it comprehensively eliminates excess reactive oxygen species (ROS) in the body, building a strong defense for cellular health and delaying the aging process.
In skin tissue, factors such as ultraviolet radiation and environmental pollution cause a large accumulation of ROS in skin cells, triggering lipid peroxidation. Lipid peroxidation leads to the oxidation of lipid components in cell membranes, producing harmful substances such as malondialdehyde (MDA), damaging the integrity of cell membranes, altering their fluidity and permeability, and thus affecting normal cell function. Dihydroquercetin, through its phenolic hydroxyl group in its molecular structure, actively donates hydrogen atoms to bind with ROS, reducing it to harmless water molecules or stable compounds, thereby effectively inhibiting lipid peroxidation, reducing MDA levels, and protecting the integrity of skin cell membranes.
In vitro cell experiments have provided strong evidence for the antioxidant and anti-aging effects of dihydroquercetin. Studies on fibroblasts have shown that the addition of dihydroquercetin significantly enhances their ability to synthesize collagen. Collagen is a key component for maintaining skin elasticity and firmness. With age or exposure to adverse external factors, collagen synthesis in the skin decreases while degradation increases, leading to wrinkles, sagging, and other signs of aging. Dihydroquercetin can promote collagen synthesis in fibroblasts while inhibiting the activity of matrix metalloproteinases (MMPs). MMPs are enzymes that degrade extracellular matrix components, including collagen and elastin. Increased MMP activity accelerates the degradation of collagen and elastin in the skin. Dihydroquercetin, by inhibiting MMP activity, reduces the degradation of collagen and elastin, thus effectively delaying the formation of wrinkles.
In the vascular system, oxidative stress is also a significant factor contributing to endothelial aging and atherosclerosis. Excessive reactive oxygen species (ROS) can damage vascular endothelial cells and impair normal vascular function. Dihydroquercetin can clear ROS from blood vessels, protect the integrity of vascular endothelial cells, and maintain their normal function. It can also inhibit the oxidation of low-density lipoprotein (LDL). Oxidized LDL is easily phagocytosed by macrophages, forming foam cells. These foam cells accumulate in the blood vessel wall, gradually forming atherosclerotic plaques. Dihydroquercetin reduces foam cell formation by inhibiting LDL oxidation, thus blocking the occurrence of atherosclerosis at its source and providing long-term protection for cardiovascular health.
(II) Anti-inflammatory Regulation: A Natural “Braking System” for Chronic Inflammation
Chronic inflammation is considered the root cause of many modern diseases, and dihydroquercetin has demonstrated remarkable regulatory capabilities in the field of anti-inflammation. It acts like a precise “brake system” for chronic inflammatory responses, effectively controlling the development of inflammation and maintaining the body’s healthy balance.
The nuclear factor κB (NF-κB) inflammatory pathway plays a central regulatory role in inflammatory responses. When the body is subjected to various inflammatory stimuli, NF-κB is activated, translocating from the cytoplasm to the nucleus, where it binds to specific DNA sequences and initiates the transcription of a series of inflammation-related genes, leading to the massive release of pro-inflammatory factors such as tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6). These pro-inflammatory factors trigger an inflammatory cascade, resulting in inflammatory damage to tissues and organs. Dihydroquercetin can precisely target and inhibit the NF-κB inflammatory pathway by inhibiting the activity of IκB kinase (IKK), thus preventing the phosphorylation and degradation of IκB protein. IκB protein is an inhibitory protein of NF-κB; under normal circumstances, IκB binds to NF-κB, rendering it inactive. When IκB is phosphorylated and degraded, NF-κB is released and activated. Dihydroquercetin, by maintaining the stability of IκB protein and blocking the nuclear translocation of NF-κB, reduces the transcription of inflammatory genes and decreases the release of pro-inflammatory factors such as TNF-α and IL-6, effectively inhibiting the inflammatory response.
In animal models of rheumatoid arthritis, treatment with dihydroquercetin significantly reduced joint swelling. Rheumatoid arthritis is an autoimmune disease characterized by joint inflammation and destruction, with inflammation playing a crucial role in joint damage. Dihydroquercetin, by inhibiting inflammatory pathways, reduces local inflammatory cell infiltration and the release of inflammatory mediators in the joints, thereby alleviating joint swelling and pain symptoms and playing a positive role in the progression of rheumatoid arthritis.
Dihydroquercetin also exhibits significant anti-inflammatory effects in non-alcoholic fatty liver disease (NAFLD). NAFLD is a liver disease closely related to metabolic disorders, and the intrahepatic inflammatory microenvironment plays an important role in its pathogenesis. Dihydroquercetin can reduce the level of pro-inflammatory factors in the liver, regulate the activity of immune cells in the liver, improve the inflammatory microenvironment in the liver, and reduce inflammatory damage to the liver, which is of great significance for the prevention and treatment of non-alcoholic fatty liver disease. In addition, dihydroquercetin also has potential intervention value for chronic low-grade inflammatory conditions such as metabolic syndrome and allergic diseases, providing new ideas and methods for the treatment of these diseases.
(III) Cardiovascular Protection: From Endothelial Repair to Thrombosis Prevention
Cardiovascular diseases seriously threaten human health, and dihydroquercetin, with its multi-target mechanism of action, provides comprehensive and in-depth protection for the cardiovascular system. From vascular endothelial repair to thrombosis prevention, it plays a crucial role in each link, becoming a powerful guardian of cardiovascular health.
Vascular endothelial cells are a single-celled layer on the inner wall of blood vessels. They are not only a barrier between blood and tissues but also secrete a variety of bioactive substances, playing a vital role in maintaining normal vascular function. When vascular endothelial function is impaired, it leads to a series of problems such as impaired vasodilation, increased blood viscosity, and thrombosis, thereby triggering cardiovascular diseases. Dihydroquercetin enhances the bioavailability of nitric oxide (NO), a potent vasodilator that diffuses from vascular endothelial cells to vascular smooth muscle cells. It activates guanylate cyclase, increasing intracellular cyclic guanosine monophosphate (cGMP) levels, leading to vascular smooth muscle relaxation. This improves endothelium-dependent vasodilation, reduces vascular resistance, maintains normal blood pressure, and promotes smooth blood flow.
Dihydroquercetin also demonstrates excellent efficacy in inhibiting low-density lipoprotein (LDL) oxidation. Oxidized LDL forms oxidized LDL (ox-LDL), which is highly cytotoxic. Ox-LDL can be taken up by macrophages, forming foam cells that accumulate in the vascular wall, gradually forming atherosclerotic plaques. Dihydroquercetin reduces the risk of atherosclerotic plaque formation by scavenging free radicals and inhibiting LDL oxidation.
Simultaneously, dihydroquercetin also inhibits the abnormal proliferation of vascular smooth muscle cells. In the development of atherosclerosis, vascular smooth muscle cells proliferate abnormally under various stimuli, leading to thickening of the vessel wall and narrowing of the lumen. Dihydroquercetin inhibits the proliferation of vascular smooth muscle cells by regulating cell signaling pathways, maintaining the normal structure and function of the vessel wall.
Dihydroquercetin also plays an important role in thrombosis prevention. It can reduce platelet aggregation, a key step in thrombus formation. Dihydroquercetin reduces the likelihood of platelet aggregation by interfering with intraplatelet signaling pathways, inhibiting the activity of phospholipase C (PLC) in platelets, and reducing the release of pro-aggregation substances such as adenosine diphosphate (ADP) and thromboxane A2 (TXA2). Furthermore, dihydroquercetin can inhibit the activity of coagulation factors, reducing thrombin-induced fibrinogen-to-fibrin conversion, thereby inhibiting thrombus formation. In summary, dihydroquercetin exhibits multi-target protective effects against cardiovascular and cerebrovascular diseases such as hypertension and coronary heart disease, providing comprehensive care for cardiovascular health.
(IV) Metabolic Optimization: A “Natural Regulator” of Glucose and Lipid Balance
In modern life, unhealthy dietary habits and lack of exercise have led to an increasing number of people facing metabolic disorders, such as type 2 diabetes, obesity, and metabolic syndrome. Dihydroquercetin, as a natural metabolic optimizer, can precisely regulate glucose and lipid metabolism by activating key signaling pathways, becoming an important “helper” in maintaining glucose and lipid balance.
The adenosine monophosphate-activated protein kinase (AMPK) pathway is an important energy regulation pathway in cells. When cellular energy levels decline, AMPK is activated, regulating the activity of a series of metabolic enzymes to promote the uptake and utilization of glucose by cells, while inhibiting the synthesis of fat and cholesterol to maintain cellular energy balance. Dihydroquercetin can activate the AMPK pathway; in adipocytes and skeletal muscle cells, it can promote the translocation of glucose transporter 4 (GLUT4). GLUT4 is a protein primarily responsible for transporting glucose into cells. Normally, GLUT4 is mainly found in intracellular vesicles. When cells are stimulated by insulin or other stimuli, GLUT4 is transported from inside the cell to the cell membrane surface, binds to glucose, and transports it into the cell, thereby lowering blood glucose levels. Dihydroquercetin enhances cellular glucose uptake and utilization by promoting GLUT4 translocation, improving insulin resistance and enabling cells to respond better to insulin, thus effectively lowering blood glucose levels.
Dihydroquercetin also shows excellent performance in regulating blood lipids. Animal experiments have shown that it can inhibit hepatic fat synthesis by downregulating the expression of key enzymes such as fatty acid synthase (FAS) and acetyl-CoA carboxylase (ACC), reducing the de novo synthesis of fatty acids and triglycerides. Simultaneously, dihydroquercetin can activate peroxisome proliferator-activated receptor α (PPARα), a core transcription factor regulating mitochondrial fatty acid β-oxidation. Once activated, PPARα upregulates the expression of genes such as carnitine palmitoyltransferase 1 (CPT1). CPT1 is a key enzyme for fatty acid β-oxidation in mitochondria; its upregulation accelerates fatty acid catabolism, thereby reducing fat accumulation in the liver. Furthermore, dihydroquercetin can improve the assembly and secretion of very low-density lipoprotein (VLDL), promoting the transport of triglycerides from the liver to the blood, further reducing liver fat content. In summary, dihydroquercetin has an auxiliary regulatory effect on diseases such as type 2 diabetes, obesity, and metabolic syndrome, providing a natural solution for improving metabolic health.
(V) Immune Regulation: A Bidirectional “Immune Balancer”
The immune system is an important defense against disease; however, imbalances in the immune system can trigger various health problems, such as autoimmune diseases and infectious diseases. Dihydroquercetin exhibits a unique bidirectional regulatory capacity in immune regulation, acting like a precise “immune balancer.” It can appropriately enhance or suppress the immune response based on the body’s immune status, maintaining the balance and stability of the immune system.
In the innate immune response, macrophages are important immune cells that engulf and clear pathogens, senescent cells, and other foreign substances, playing a crucial role in the body’s immune defense. Dihydroquercetin can enhance the phagocytic activity of macrophages, enabling them to more effectively recognize and engulf pathogens. It can also stimulate macrophages to secrete immune signaling molecules, such as tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β). These immune signaling molecules can activate other immune cells, enhancing the body’s immune defense capabilities.
In the adaptive immune response, T cells are one of the core cells. Imbalance in their function can lead to problems such as excessive or deficient immunity. Dihydroquercetin can inhibit excessive T cell activation and regulate the balance of the Th1/Th2 cell subsets. Th1 cells primarily participate in cellular immunity, secreting cytokines such as interferon-γ (IFN-γ), activating macrophages, and enhancing the body’s ability to clear intracellular pathogens. Th2 cells primarily participate in humoral immunity, secreting cytokines such as interleukin-4 (IL-4) and interleukin-5 (IL-5), promoting antibody production by B cells, and enhancing the body’s ability to clear extracellular pathogens. Under normal circumstances, Th1/Th2 cells are in a state of balance. When this balance is disrupted, immune-related diseases can occur. Dihydroquercetin regulates the balance of Th1/Th2 cell subsets, enabling the immune system to respond more precisely to different pathogen invasions, avoiding either over- or under-immune reactions.
Preliminary studies show that dihydroquercetin has the potential to improve autoimmune diseases such as rheumatoid arthritis and allergic rhinitis. In rheumatoid arthritis, the immune system mistakenly attacks joint tissues, leading to joint inflammation and damage. Dihydroquercetin plays a certain role in inhibiting the progression of rheumatoid arthritis by regulating the function of immune cells, inhibiting the release of inflammatory factors, and reducing joint inflammation. In allergic rhinitis, the body produces an excessive immune response to allergens; dihydroquercetin alleviates allergy symptoms by regulating the activity of Th2 cells and reducing the secretion of allergy-related cytokines. Although the specific clinical mechanisms of dihydroquercetin in immune regulation still need further verification, its bidirectional regulatory capacity provides new directions and hope for the treatment of immune-related diseases.
Scientific Application and Safety Boundaries: A Practical Guide from Supplementation to Intervention
(I) Daily Dietary Supplementation Strategies
In daily life, we can cleverly integrate dihydroquercetin into our diet through reasonable dietary choices, providing continuous support for our health. Onions are a common food rich in dihydroquercetin. When eaten raw, they retain the maximum activity of dihydroquercetin. Raw onion salad is not only simple to prepare but also preserves the original flavor and nutrients of the onion, allowing us to better absorb dihydroquercetin. Apples are also a common fruit in our daily diet. Eating apples with the peel allows for the intake of more dihydroquercetin. Apple peels are rich in various nutrients, including dihydroquercetin. After washing thoroughly, eating the apple with the peel allows us to fully utilize its nutritional value. Dark chocolate is also a good choice. When the cocoa content is greater than 70%, dark chocolate contains a certain amount of dihydroquercetin. Consuming dark chocolate in moderation not only satisfies the taste buds but also replenishes the body with dihydroquercetin. In addition, pine needle tea is also a beverage rich in dihydroquercetin. By brewing pine needle tea, we can infuse the dihydroquercetin from the pine needles into the beverage, making it convenient for daily consumption. Through the reasonable combination of these natural ingredients, we can ingest approximately 50-100mg of dihydroquercetin daily.
Besides obtaining dihydroquercetin from natural foods, dietary supplements are also an effective way to supplement it. When choosing dietary supplements, standardized extracts should be prioritized. These extracts typically have a purity of over 98%, ensuring a high concentration of dihydroquercetin in the supplement, thereby improving its effectiveness. To reduce gastrointestinal irritation, it is recommended to take dihydroquercetin supplements after meals. After a meal, with food present in the gastrointestinal tract, taking supplements at this time can reduce the direct irritation of the supplements to the gastrointestinal mucosa, lower the risk of gastrointestinal discomfort, and allow the body to absorb the nutrients of dihydroquercetin more comfortably.
(II) Warnings for Special Populations
For pregnant and breastfeeding women, due to the relative scarcity of safety data on dihydroquercetin in these groups, it is generally not recommended for pregnant and breastfeeding women to take dihydroquercetin on their own to minimize potential adverse effects on the fetus or infant. If there is a need to take it under special circumstances, it is essential to strictly follow the professional guidance of a doctor. The doctor will comprehensively assess the benefits and risks based on the individual’s specific situation and provide the most appropriate advice and medication plan.
People taking anticoagulants also need to pay extra attention. Dihydroquercetin may interact with anticoagulants such as warfarin, thereby affecting the efficacy of the drugs and even increasing the risk of adverse reactions such as bleeding. Therefore, individuals in this category must consult a doctor before considering taking dihydroquercetin. The doctor will carefully assess whether dihydroquercetin can be used concurrently based on the patient’s condition, medication history, and overall health, and will provide corresponding adjustment suggestions.
For some severely ill individuals, such as rectal cancer patients over 81 years of age, due to a lack of sufficient clinical data to support the safety and efficacy of dihydroquercetin in this population, self-medication with dihydroquercetin is prohibited. When facing serious illnesses, the treatment plan developed by the clinician should be prioritized. These plans are based on extensive clinical research and practical experience, maximizing the patient’s treatment effectiveness and safety.
(III) Potential Risks and Monitoring Points
Although dihydroquercetin is beneficial to human health when used appropriately, long-term use at high doses, exceeding 500mg daily, may trigger a series of gastrointestinal discomfort symptoms. Nausea is one of the more common symptoms. This is because high doses of dihydroquercetin may stimulate nerve endings in the gastrointestinal tract, causing stomach discomfort and triggering nausea. Diarrhea is also a possible symptom. High doses of dihydroquercetin may affect normal gastrointestinal motility and digestive function, leading to reduced water absorption in the intestines, resulting in loose stools and diarrhea. To detect and prevent these potential risks from causing more serious health consequences, regular monitoring of liver and kidney function is recommended. The liver and kidneys are important metabolic and excretory organs in the human body. The metabolism and excretion of dihydroquercetin in the body require the liver and kidneys. Long-term use of high doses may increase the burden on the liver and kidneys. Regular monitoring of liver and kidney function can detect signs of liver and kidney damage in a timely manner, allowing for adjustments to the dosage or appropriate treatment.
People with allergies need to be especially cautious when using dihydroquercetin. A skin sensitivity test should be performed before first use. Apply a small amount of dihydroquercetin product to sensitive areas such as the inside of your wrist or behind your ear, and observe for 24-48 hours to see if any allergic reactions such as itching, rash, or erythema occur. If no discomfort occurs during the test, dihydroquercetin can be used cautiously under the guidance of a doctor. If an allergic reaction occurs, discontinue use immediately and seek medical attention promptly. Furthermore, avoid taking dihydroquercetin with alcohol. Alcohol affects liver metabolism and increases the burden on the liver. Taking dihydroquercetin and alcohol simultaneously may further increase the metabolic burden on the liver, affecting the normal metabolism and excretion of dihydroquercetin and increasing the risk of adverse reactions.
Future Prospects: Translational Potential from Laboratory to Clinical
Although current research on dihydroquercetin is largely focused on animal models and in vitro experiments, its preliminary findings in several fields have already revealed its enormous application potential and broad development prospects.
In the field of anti-tumor therapy, numerous studies have shown that dihydroquercetin has inhibitory effects on various cancer cells. Taking rectal cancer cells as an example, related experiments have found that dihydroquercetin can effectively inhibit the proliferation of rectal cancer cells and induce apoptosis. Its mechanism of action may be related to regulating signaling pathways within cancer cells and inhibiting tumor angiogenesis. Although these studies are still in the basic stage, they provide new directions and ideas for the future development of novel anti-cancer drugs.
In antiviral therapy, dihydroquercetin also exhibits unique effects. Studies have found that it can enhance the sensitivity of antibiotics to streptococci, meaning that dihydroquercetin may be used in combination with antibiotics to improve treatment efficacy, reduce antibiotic dosage, and thus reduce antibiotic side effects. Furthermore, for some viral infectious diseases, dihydroquercetin enhances the body’s resistance to viruses by regulating the immune response, providing a new strategy for antiviral treatment.
Neuroprotection is another important area of dihydroquercetin research. With the increasing aging of the population, the incidence of neurodegenerative diseases such as Alzheimer’s disease and Parkinson’s disease is gradually rising. These diseases severely affect the quality of life of patients and place a heavy burden on families and society. Current research shows that dihydroquercetin can exert neuroprotective effects through multiple pathways, such as scavenging reactive oxygen species in the brain and reducing oxidative stress damage to neurons; inhibiting the inflammatory response triggered by microglia activation and reducing the level of inflammatory factors; and regulating mitochondrial function in the brain and improving energy metabolism disorders. These mechanisms of action are closely related to the core links in the pathogenesis of neurodegenerative diseases, bringing hope for slowing the progression of neurodegenerative diseases such as Alzheimer’s.
With the gradual advancement of Phase III clinical trials, dihydroquercetin is expected to be translated from the laboratory to the clinical, becoming a core component of precision nutritional intervention and functional medicine. Precision nutrition intervention involves developing personalized nutritional plans based on an individual’s genes, metabolism, lifestyle, and other factors to prevent and treat diseases. Dihydroquercetin, a natural compound with diverse biological activities, can provide natural and effective solutions for various individual health problems, such as oxidative stress-related chronic diseases. In functional medicine, dihydroquercetin may also play an important role, improving the body’s internal environment and promoting health recovery by regulating physiological functions.
With its unique molecular structure and multi-functional biological activities, dihydroquercetin serves as a bridge connecting natural plant components with modern health needs. When applied rationally under scientific guidance, this natural antioxidant is opening new possibilities for combating aging, inflammation, and metabolic diseases. We have reason to expect it to play a greater role in the future of medicine and health, making significant contributions to human health.
