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Dihydromyricetin (DHM or DMY) is a flavonoid derived from natural sources with a range of confirmed biological benefits. It exhibits anti-inflammatory, antioxidant, anti-tumor, and anti-viral activities. DHM is recognized for its high biosafety, making it a promising subject for further research. This article offers a comprehensive overview of DHM's pharmacological properties, mechanisms, and recent research developments in the cardiovascular, urinary, digestive, nervous, and respiratory systems. The review summarizes DHM's biological effects and associated signaling pathways, providing novel insights for its clinical application. [ABSTRACT FROM AUTHOR]

Dihydromyricetin (DMY), as the main active ingredient in Ampelopsis grossedentata, is a naturally occurring flavonoid that has attracted extensive attention for its multiple biological activities. For the quick and accurate measurement of DMY, a novel electrochemical sensor based on a glassy carbon electrode (GCE) modified with a cobalt metal-organic framework (Co-MOF) was proposed in this work. The Co-MOF was synthesized via a single-step hydrothermal process using Co(NO3)2·6H2O. Fourier infrared spectroscopy, X-ray photoelectron spectroscopy and scanning electron microscopy were used to study the morphology and structure of the synthesized Co-MOF. Utilizing differential pulse voltammetry and cyclic voltammetry methods, the effectiveness of DMY electro-oxidation on the Co-MOF/GCE was examined. The results showed that, in comparison to the bare GCE, the electro-oxidation peak current of DMY was considerably increased by the Co-MOF/GCE. The detection limit was 0.07 μM, and the peak current demonstrated two linear relationships in the ranges of 0.2−20 μM and 20−100 μM, with the linear equations of Ip (μA) = 0.4729c (μM) + 1.0822 (R2 = 0.9913) and Ip (μA) = 0.0939c (μM) + 8.4178 (R2 = 0.9971), respectively. The average DMY content in Ampelopsis grossedentata samples was measured to be 3.275 μM, with a good recovery of 108.27% and a relative standard deviation value of 3.46%. The proposed method is simple, rapid and sensitive and can be used for the determination of DMY in Ampelopsis grossedentata. [ABSTRACT FROM AUTHOR]

Background: Ampelopsis grossedentata, vine tea, which is the tea alternative beverages in China. In vine tea processing, a large amount of broken tea is produced, which has low commercial value. Methods: This study investigates the influence of different extraction methods (room temperature water extraction, boiling water extraction, ultrasonic-assisted room temperature water extraction, and ultrasonic-assisted boiling water extraction, referred to as room temperature water extraction (RE), boiling water extraction (BE), ultrasonic assistance at room temperature water extraction (URE), and ultrasonic assistance in boiling water extraction (UBE)) on the yield, dihydromyricetin (DMY) content, free amino acid composition, volatile aroma components, and antioxidant properties of vine tea extracts. Results: A notable influence of extraction temperature on the yield of vine tea extracts (P < 0.05), with BE yielding the highest at 43.13 ± 0.26%, higher than that of RE (34.29 ± 0.81%). Ultrasound-assisted extraction significantly increased the DMY content of the extracts (P < 0.05), whereas DMY content in the RE extracts was 59.94 ± 1.70%, that of URE reached 66.14 ± 2.78%. Analysis revealed 17 amino acids, with L-serine and aspartic acid being the most abundant in the extracts, nevertheless ultrasound-assisted extraction reduced total free amino acid content. Gas chromatography-mass spectrometry analysis demonstrated an increase in the diversity and quantity of compounds in the vine tea water extracts obtained through ultrasonic-assisted extraction. Specifically, 69 and 68 volatile compounds were found in URE and UBE extracts, which were higher than the number found in RE and BE extracts. In vitro, antioxidant activity assessments revealed varying antioxidant capacities among different extraction methods, with RE exhibiting the highest DPPH scavenging rate, URE leading in ABTS+ free radical scavenging, and BE demonstrating superior ferric ion reducing antioxidant activity. Conclusion: The findings suggest that extraction methods significantly influence the chemical composition and antioxidant properties of vine tea extracts. Ultrasonic-assisted extraction proved instrumental in elevating the DMY content in vine tea extracts, thereby enriching its flavor profile while maintaining its antioxidant properties. [ABSTRACT FROM AUTHOR]

Multiple myeloma (MM) is a plasma cell malignancy and remains incurable as it lacks effective curative approaches; thus, novel therapeutic strategies are desperately needed. The study aimed to explore the therapeutic role of dihydromyricetin (DHM) in MM and explore its mechanisms. Human MM and normal plasma samples, human MM cell lines, and normal plasma cells were used for in vitro experiments. Cell counting kit-8 (CCK-8), flow cytometry, and trans-well assays were performed for the assessment of cell viability, apoptosis, migration, and invasion, respectively. Quantitative real-time polymerase chain reaction (qRT-PCR) was employed to assess the mRNA expression of signal transducer and activator of transcription 1 (STAT1) and retinoic acid-inducible gene I (RIG-I). Western blotting was employed to assess E-cadherin, N-cadherin, signal transducer, STAT1, p-STAT1, and RIG-I protein expression. A tumor xenograft model was used for in vivo experiments. Here, dihydromyricetin (DHM) dose-dependently restrained viability, apoptosis, migration, and invasion, and facilitated apoptosis of U266 cells. After DHM treatment, the E-cadherin level was increased and the N-cadherin level was decreased in U266 and RPMI-8226 cells, suggesting the inhibitory effects of DHM on epithelial-mesenchymal transition (EMT) in MM. Besides, the levels of p-STAT1/STAT1 and RIG-I were down-regulated in MM. However, the STAT1 inhibitor fludarabine undid the suppressive effect of DMH on the malignant characteristics of U266 cells. Also, DHM inhibited MM tumor growth and EMT, and activated STAT1/RIG-I pathway in vivo. Collectively, this study first revealed that DHM can restrain EMT and tumor growth in MM by activating STAT1/RIG-I signaling, which provides a novel drug for the treatment of MM. Graphic Abstract Ampelopsis grossedentata) on multiple myeloma by activating STAT1/RIG-I axis" class="showdlg" rel-p="photosdshow" style="max-width:100%; margin: 0px auto; cursor: pointer" /> [ABSTRACT FROM AUTHOR]

An oxidising and substituting one-pot reaction strategy has been developed to synthesise dihydromyricetin derivatives with the aim of enhancing the inhibitory activity of dihydromyricetin against SARS-CoV-2. Different ω-methoxy-ω-oxeylkyl was introduced in C7-OH site and yielded eight analogs, all of them showed good inhibitory activity against SARS-CoV-2 3CLpro with IC50 values ranging from 0.72 to 2.36 μM. In the Vero E6-cell, compound 3 has a good activity of anti-SARS-CoV-2 virus (Omicron virus BA.5) in the prevention model, with an EC50 of 15.84 μM, and so do compound 10 in the therapeutic model, with an EC50 of 11.52 μM. The results suggest that the introduction of long chain ω-oxeylkyl at C7-OH facilitate the inhibition of viral replication in the therapeutic model, which is consistent with the binding energies predicted from molecular docking conclusions. It implies that dihydromyricetin derivatives have the potential to become effective inhibitors of SARS-CoV-2 Omicron and other viruses. [ABSTRACT FROM AUTHOR]

Sepsis complicated by acute kidney injury (AKI) carries an extremely high mortality rate. The present study aimed to investigate the protective effect and underlying mechanism of dihydromyricetin (DHM) on human renal tubular epithelial cells (HK2) during AKI. To simulate an in vitro model of AKI, HK2 cells were treated with lipopolysaccharide (LPS) and divided into four groups: Control, LPS, LPS+DHM, and LPS+DHM+si-HIF-1α. The cellular viability of HK2 cells was determined by the CCK-8 assay after treatment with LPS and DHM (60 μmol/L). The expression of Bcl-2, Bax, Cleaved Caspase-3, and HIF-1α was measured by Western blotting. The expression of Bcl-2, Bax, and HIF-1α mRNA was assessed by PCR. The apoptosis rate of each group was determined by flow cytometry, while different kits were used to measure the levels of MDA, SOD, and LDH in each group of HK2 cells. DHM was found to increase the expression of HIF-1α in HK2 cells after treatment with LPS. the expression of HIF-1α mRNA and protein, Cleaved Caspase-3, Bax protein, MDA and LDH levels, and apoptosis rate were significantly decreased, while Bcl-2 protein, cell viability, and SOD activity were markedly increased in the LPS+DHM group compared with the LPS and LPS+DHM+si-HIF-1α groups. Thus, DHM can reduce apoptosis and oxidative stress damage in HK2 cells by increasing HIF-1α expression after LPS treatment. DHM may be a treatment for AKI, but in vitro studies must be validated in animal models and clinical trials before drawing conclusions. Caution must be exercised in interpreting in vitro results. [ABSTRACT FROM AUTHOR]

The gut microbiota may help mitigate bone loss linked to postmenopausal osteoporosis by affecting the immune and inflammatory responses and the gut-bone axis. Dihydromyricetin (DMY), a natural flavonoid, has some anti-inflammatory and antioxidant properties. This study aimed to investigate the mechanisms underlying the amelioration of bone loss in ovariectomized (OVX) mice treated with various doses of DMY. Eight-week-old C57/BL6 mice underwent ovariectomy and received varying DMY doses over 8 weeks. Thereafter, femoral bone microarchitecture, serum biomarker levels, and colon samples were analyzed to assess bone metabolism and inflammatory and hormonal responses. Fecal samples were subjected to 16S rDNA sequencing, and short-chain fatty acids were quantified. An untargeted metabolomics approach was applied to both serum and fecal samples to investigate alterations in the intestinal microbiota and metabolic profiles following DMY treatment in the OVX mice. The results show high-dose DMY has anti-osteoporotic effects. Compared to the OVX group, the DMY-treated group showed enhanced bone mineral density and reduced inflammation and colonic damage levels. The DMY treatment altered the gut microbiota composition, including the relative abundances at both the phylum and genus levels. In addition, DMY treatment increased the production of acetate and propionate. Metabolomic analysis revealed differential regulation of 37 and 70 metabolites in the serum and feces samples, respectively, in the DMY-treated group compared to those in the OVX group, affecting the serotonergic signaling, arachidonic acid metabolism, and unsaturated fatty acid biosynthesis pathways. In conclusion, these findings indicate that DMY can ameliorate bone loss in OVX mice via the gut-bone axis. DMY can ameliorate bone loss in OVX mice via the gut-bone axis. [ABSTRACT FROM AUTHOR]

Introduction In recent years, a growing number of clinical and biological studies have shown that patients with type 2 diabetes mellitus (T2DM) are at increased risk of developing Parkinson's disease (PD). Prolonged exposure to hyperglycemia results in abnormal glucose metabolism, which in turn causes pathological changes similar to PD, leading to selective loss of dopaminergic neurons in the compact part of the substantia nigra. Dihydromyricetin (DHM) is a naturally occurring flavonoid with various biological activities including antioxidant and hepatoprotective properties. In this study, the effect of DHM on high glucose-induced dopaminergic neuronal damage was investigated. Methods The potential modulatory effects of DHM on high glucose-induced dopaminergic neuronal damage and its mechanism were studied. Results DHM ameliorated high glucose-induced dopaminergic neuronal damage and autophagy injury. Inhibition of autophagy by 3-methyladenine abrogated the beneficial effects of DHM on high glucose-induced dopaminergic neuronal damage. In addition, DHM increased levels of p-AMP-activated protein kinase (AMPK) and phosphorylated UNC51-like kinase 1. The AMPK inhibitor compound C eliminated DHM-induced autophagy and subsequently inhibited the ameliorative effects of DHM on high glucose-induced dopaminergic neuronal damage. Discussion DHM ameliorates high glucose-induced dopaminergic neuronal damage by activating the AMPK-autophagy pathway. [ABSTRACT FROM AUTHOR]

Vine tea extract (VTE), from the traditional Chinese herbal tea, was added to reconstituted skimmed milk; the mixture was fermented with Lacticaseibacillus casei, and fermentation characteristics, flavonoid content, antioxidant capacity (AOC), and viability of L. casei were measured. 2 mg/mL VTE promoted L. casei growth and 8 mg/mL VTE inhibited growth, an effect consistent with observed pH changes. Total flavonoid content and AOC increased with increasing VTE dosage. Dihydromyricetin was partially metabolized during fermentation and accounted for most of the antioxidant function of VTE. 2 mg/mL VTE was optimal for maintenance of probiotic culture and pH stability during cold storage and improved AOC during product shelf life. VTE has the potential to increase the health benefits of probiotic dairy products, and the resulting mixture may be suitable to use as a daily milk‐based health drink. [ABSTRACT FROM AUTHOR]

Summary: α‐Glycosidase, a critical therapeutic target in type 2 diabetes mellitus (T2DM), can be modulated by inhibitors to reduce postprandial blood glucose levels. This study investigated the inhibitory effects of vine tea (Ampelopsis grossedentata) and its key compounds on α‐glycosidase. The results demonstrated that fifteen varieties of vine tea extracts inhibited α‐glycosidase in a dose‐dependent manner, with IC50 values ranging from 5.25 to 35.8 μg mL−1. HPLC analysis revealed dihydromyricetin (DHM) as the main compound in vine tea, with an IC50 value of 262.50 μM. Notably, the synergistic combination of DHM and the antidiabetic drug acarbose (ABS) significantly enhanced inhibitory effectiveness, with the optimal ratio (1:125) yielding a potentiation index (CI) of 0.09. Fluorescence and molecular docking analyses supported the hypothesis that DHM enhanced ABS's inhibitory effect through complex formation and specific interactions, offering a promising option for safer and more effective diabetes therapy. [ABSTRACT FROM AUTHOR]

The combination of proteins with polysaccharides and polyphenols is expected to improve their physicochemical and functional properties. In this study, a novel plant-based antioxidant emulsifier was formed by soybean protein isolate (SPI), inulin (INU), and dihydromyricetin (DMY). Based on the binary system of SPI/INU, we focused on exploring the effect of the DMY concentration (0.5 mg/mL~2.5 mg/mL) on the formation and properties of the ternary complex. The structure, interaction mechanism, and interfacial and functional properties of the ternary complex were investigated. The results indicate that compared to the SPI/INU binary complex, the SPI/INU/DMY ternary complex had a significant decrease in particle size (~100 nm) and a slight decrease in absolute zeta potential. The SPI/INU binary complex with DMY mainly interacted by hydrogen bonding and hydrophobic interactions. Due to the incorporation of DMY, the structure of SI was denser and more flexible. The ternary complex exhibited an ideal three-phase contact angle and demonstrated better foaming and antioxidant ability. Additionally, compared to SPI/INU, the ternary complex had a significant improvement in EAI. These results provide a strategy for polyphenols to modify the structure, interfacial properties, and functions of protein/polysaccharide complexes. This provides a potential reference for the preparation of more ternary complexes with excellent emulsifying and antioxidant properties for application in emulsions. [ABSTRACT FROM AUTHOR]

In this paper, the molecular geometry of dihydromyricetin was optimized based on density flooding theory (DFT)using B3LYP flooding combined with 6-31G group, based on which the active sites of dihydromyricetin molecules were calculated using water as solvent and the infrared spectra was analyzed. The electrostatic potential results showed that the nucleophilic active site of dihydromyricetin is located near the phenolic hydroxyl atom (H23) ; while the electrophilic active site is located in and near the oxygen atom (O32) . The results of frontline molecular orbital studies indicate that the highest occupied orbitals (HOMO) of dihydromyricetin molecules are located near ketone oxygen (O32)and hydroxyl oxygen (O20), indicating that these sites are susceptible to reaction with electrophilic reagents. And the lowest occupied orbitals (LUMO) are located in the carbon atom (C12, C13, C14) region, indicating that these regions can react with nucleophilic reagents. The results of the simplified Fukui function (f) confirm that the electrophilic activity of the f-value of the oxygen atom reagents. The results of the simplified Fukui function (f) confirm that the electrophilic activity of the f-value of the oxygen atom located in the C-O-C bond is larger than those of the oxygen atom in other sites; while the f+ value of the carbon atom located in C8 is larger, so the nucleophilic activity is stronger in this site. The infrared spectral data of dihydromyricetin obtained by theoretical calculations do not differ much from those obtained experimentally, which indicates that the theoretical calculations may be reliable. Thus, it provides some theoretical reference for the experimental and theoretical studies of the relationship between the structure and properties of dihydromyricetin. [ABSTRACT FROM AUTHOR]

This study aimed to investigate the effect of oxidized dihydromyricetin (oDMY) on the gel properties of silver carp (Hypophthalmichthys molitrix) surimi. The changes in gel strength, rheological properties, water-holding capacity, microstructure, protein secondary structure, particle size distribution, color, and sensory properties of surimi gels were analyzed after adding different concentrations (0%, 0.15%, 0.30%, 0.45%, 0.60%) of oDMY. The results showed that the addition of oDMY increased the relative content of β-sheet proteins during the gel formation process, leading to larger particle size due to protein aggregation, and consequently resulting in a denser gel network structure with smaller pores. Furthermore, the water-holding capacity of the surimi gels was improved by the addition of oDMY. As the concentration of oDMY increased, the breaking force and deformation of the surimi gels increased, especially at the concentration of 0.45%, which exhibited the most significant enhancement in breaking force. Dynamic rheological tests further demonstrated that oDMY had a certain delaying effect on gel deterioration. The addition of oDMY resulted in a decrease in whiteness of the surimi gels. However, at lower concentrations, the impact on color remained within an acceptable range, and oDMY positively contributed to the flavor improvement of the surimi gels. Overall, the addition of 0.45% oDMY effectively improved the characteristics of silver carp surimi gels, providing valuable reference for the development of novel surimi products.

Abstract Background NOD-like receptor protein 3 (NLRP3) inflammasome activation is indispensable for atherogenesis. Mitophagy has emerged as a potential strategy to counteract NLRP3 inflammasome activation triggered by impaired mitochondria. Our previous research has indicated that dihydromyricetin, a natural flavonoid, can mitigate NLRP3-mediated endothelial inflammation, suggesting its potential to treat atherosclerosis. However, the precise underlying mechanisms remain elusive. This study sought to investigate whether dihydromyricetin modulates endothelial mitophagy and inhibits NLRP3 inflammasome activation to alleviate atherogenesis, along with the specific mechanisms involved. Methods Apolipoprotein E-deficient mice on a high-fat diet were administered daily oral gavages of dihydromyricetin for 14 weeks. Blood samples were procured to determine the serum lipid profiles and quantify proinflammatory cytokine concentrations. Aortas were harvested to evaluate atherosclerotic plaque formation and NLRP3 inflammasome activation. Concurrently, in human umbilical vein endothelial cells, Western blotting, flow cytometry, and quantitative real-time PCR were employed to elucidate the mechanistic role of mitophagy in the modulation of NLRP3 inflammasome activation by dihydromyricetin. Results Dihydromyricetin administration significantly attenuated NLRP3 inflammasome activation and vascular inflammation in mice on a high-fat diet, thereby exerting a pronounced inhibitory effect on atherogenesis. Both in vivo and in vitro, dihydromyricetin treatment markedly enhanced mitophagy. This enhancement in mitophagy ameliorated the mitochondrial damage instigated by saturated fatty acids, thereby inhibiting the activation and nuclear translocation of NF-κB. Consequently, concomitant reductions in the transcript levels of NLRP3 and interleukin-1β (IL-1β), alongside decreased activation of NLRP3 inflammasome and IL-1β secretion, were discerned. Notably, the inhibitory effects of dihydromyricetin on the activation of NF-κB and subsequently the NLRP3 inflammasome were determined to be, at least in part, contingent upon its capacity to promote mitophagy. Conclusion This study suggested that dihydromyricetin may function as a modulator to promote mitophagy, which in turn mitigates NF-κB activity and subsequent NLRP3 inflammasome activation, thereby conferring protection against atherosclerosis.

Objective To investigate the protective effect of dihydromyricetin (DMY) against injury of primary hip-pocampal neurons caused by ferric ammonium citrate (FAC) and its mechanism. Methods Primary hippocampal neurons were collected from 24-hour neonatal Sprague-Dawley rats for in vitro culture, and CCK-8 assay was used to measure the viability of primary hippocampal neurons treated with different concentrations of DMY and determine the administration concentration of DMY. Primary hippocampal neurons were divided into control group (H group), 100 mmol/L DMY treatment group (I group), 250 mmol/L FAC treatment group (J group), and 100 mmol/L DMY+250 mmol/L FAC treatment group (K group). Flow cytometry was used to measure the content of reactive oxygen species (ROS) in each group; colorimetry was used to measure the content of malondialdehyde (MDA) in each group; Western blot was used to measure the protein expression levels of nuclear factor erythroid 2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1), and glutathione peroxidase 4 (GPX4) in each group. Results CCK-8 assay showed the highest viability of primary hippocampal neurons at the concentration of 100 mmol/L for DMY (F=9.95,P

The gut microbiota may help mitigate bone loss linked to postmenopausal osteoporosis by affecting the immune and inflammatory responses and the gut-bone axis. Dihydromyricetin (DMY), a natural flavonoid, has some antiinflammatory and antioxidant properties. This study aimed to investigate the mechanisms underlying the amelioration of bone loss in ovariectomized (OVX) mice treatedwith various doses of DMY. Eight-week-old C57/BL6mice underwent ovariectomy and received varying DMY doses over 8 weeks. Thereafter, femoral bone microarchitecture, serumbiomarker levels, and colon samples were analyzed to assess bone metabolism and inflammatory and hormonal responses. Fecal samples were subjected to 16S rDNA sequencing, and short-chain fatty acids were quantified. An untargetedmetabolomics approachwas applied to both serum and fecal samples to investigate alterations in the intestinal microbiota and metabolic profiles following DMY treatment in the OVX mice. The results show high-dose DMY has anti-osteoporotic effects. Compared to the OVX group, the DMY-treated group showed enhanced bone mineral density and reduced inflammation and colonic damage levels. The DMY treatment altered the gut microbiota composition, including the relative abundances at both the phylum and genus levels. In addition, DMY treatment increased the production of acetate and propionate. Metabolomic analysis revealed differential regulation of 37 and 70 metabolites in the serum and feces samples, respectively, in the DMY-treated group compared to those in the OVX group, affecting the serotonergic signaling, arachidonic acid metabolism, and unsaturated fatty acid biosynthesis pathways. In conclusion, these findings indicate thatDMY can ameliorate bone loss in OVXmice via the gut-bone axis. [ABSTRACT FROM AUTHOR]

Background: Nonalcoholic fatty liver disease (NAFLD) poses a risk for numerous metabolic diseases. To date, the U.S. Food and Drug Administration has not yet approved any medications for the treatment of NAFLD, for which developing therapeutic drugs is urgent. Dihydromyricetin (DMY), the most abundant flavonoid in vine tea, has been shown to be hepatoprotective. Its application was limited by low bioavailability in vivo; Methods: In order to improve the bioavailability of DMY and achieve liver-targeted delivery, we designed a DMY-loaded stiff-soft hybrid biomimetic nano drug delivery system (DMY-hNE). The in vivo absorption, distribution, pharmacokinetic profiles, and anti-NAFLD efficacy of DMY-hNE were studied; Results: DMY-hNE was composed of a stiff core and soft shell, which led to enhanced uptake by gastrointestinal epithelial cells and increased penetration of the mucus barrier, thus improving the in vivo absorption, plasma DMY concentration, and liver distribution versus free DMY. In an early NAFLD mouse model, DMY-hNE effectively ameliorated fatty lesions accompanied with reduced lipid levels and liver tissue inflammation; Conclusions: These findings suggested that DMY-hNE is a promising platform for liver drug delivery and treatment of hepatopathy. [ABSTRACT FROM AUTHOR]

Skin aging is driven by a complex set of cellular pathways. Among these, epigenetic mechanisms have garnered particular attention, because of their sensitivity to environmental and lifestyle factors. DNA methylation represents the longest known and best understood epigenetic mechanism. We explain how DNA methylation might function as an interface between the environment and the genome of human skin. Exposures to different environmental factors and lifestyles are known to modulate age‐related methylation patterns, as illustrated by their effect on DNA methylation clocks. Human skin provides a particularly well‐suited tissue for understanding age‐related methylation changes and it has been shown recently that modulation of DNA methylation can induce skin rejuvenation. We explain how the use of mildly demethylating agents can be safeguarded to ensure the specific removal of age‐related DNA methylation changes. We also identify important areas of future research, leading to a deeper understanding of the mechanisms that drive epigenetic aging and to the development of further refined intervention strategies. [ABSTRACT FROM AUTHOR]

The onset of Alzheimer's disease (AD) is significantly influenced by oxidative stress. Trace element selenium (Se) can be incorporated into selenoproteins to participate in redox regulation. In our previous study, it was found that brain-targeting chlorogenic acid-modified selenium nanoparticles (SeNPs) could effectively relieve oxidative stress in AD. However, the main mechanism of polyphenol-decorated SeNPs on antioxidant enzymes such as glutathione peroxidase is still unknown. Dihydromyricetin (DMY) is one polyphenol that has neuroprotective effects through antioxidant activities. In this study, chitosan (CS) was introduced as a stabilizer for the synthesis of a brain-targeted peptide (Tg: TGNYKALHPHNG) and DMY-modified SeNPs (Tg-CS/DMY@SeNPs). Tg-CS/DMY@SeNPs could improve the solubility of DMY and exhibited better free radical scavenging ability than DMY. Meanwhile, Tg-CS/DMY@SeNPs significantly enhanced the activity of antioxidant enzymes, which effectively inhibited ROS accumulation in Aβ aggregate-induced PC12 cells. More importantly, Tg-CS/DMY@SeNPs could activate the Nrf2/Keap-1 signaling pathway to regulate the activity of antioxidant enzymes, especially selenophenase glutathione peroxidase in the brain and liver of APP/PS1 mice. In that case, Tg-CS/DMY@SeNPs also prevented oxidative damage-induced apoptosis by inhibiting the Caspase-3 signaling pathway in the brain and liver of APP/PS1 mice. Finally, Tg-CS/DMY@SeNPs remarkably improved cognitive disorders in the APP/PS1 mice. These results indicated that Tg-CS/DMY@SeNPs exhibited promising therapeutic effects in the antioxidant therapy of AD. [ABSTRACT FROM AUTHOR]

Sevoflurane (Sev) is a commonly used inhalation anaesthetic that has been shown to cause hippocampus dysfunction through multiple underlying molecular processes, including mitochondrial malfunction, oxidative stress and inflammation. Dihydromyricetin (DHM) is a 2,3‐dihydroflavonoid with various biological properties, such as anti‐inflammation and anti‐oxidative stress. The purpose of this study was to investigate the effect of DHM on Sev‐induced neuronal dysfunction. HT22 cells were incubated with 10, 20 and 30 μM of DHM for 24 h, and then stimulated with 4% Sev for 6 h. The effects and mechanism of DHM on inflammation, oxidative stress and mitochondrial dysfunction were explored in Sev‐induced HT22 cells by Cell Counting Kit‐8, flow cytometry, enzyme‐linked immunosorbent assay, reverse transcription‐quantitative polymerase chain reaction, colorimetric detections, detection of the level of reactive oxygen species (ROS), mitochondrial ROS and mitochondrial membrane potential (MMP), immunofluorescence and western blotting. Our results showed that DHM increased Sev‐induced cell viability of HT22 cells. Pretreatment with DHM attenuated apoptosis, inflammation, oxidative stress and mitochondrial dysfunction in Sev‐elicited HT22 cells by remedying the abnormality of the indicators involved in these progresses, including apoptosis rate, the cleaved‐caspase 3 expression, as well as the level of tumour necrosis factor α, interleukin (IL)‐1β, IL‐6, malondialdehyde, superoxide dismutase, catalase, ROS, mitochondrial ROS and MMP. Mechanically, pretreatment with DHM restored the Sev‐induced the expression of SIRT1/FOXO3a pathway in HT22 cells. Blocking of SIRT1 counteracted the mitigatory effect of DHM on apoptosis, inflammation, oxidative stress and mitochondrial dysfunction in Sev‐elicited HT22 cells. Collectively, pretreatment with DHM improved inflammation, oxidative stress and mitochondrial dysfunction via SIRT1/FOXO3a pathway in Sev‐induced HT22 cells. [ABSTRACT FROM AUTHOR]

Background: NOD-like receptor protein 3 (NLRP3) inflammasome activation is indispensable for atherogenesis. Mitophagy has emerged as a potential strategy to counteract NLRP3 inflammasome activation triggered by impaired mitochondria. Our previous research has indicated that dihydromyricetin, a natural flavonoid, can mitigate NLRP3-mediated endothelial inflammation, suggesting its potential to treat atherosclerosis. However, the precise underlying mechanisms remain elusive. This study sought to investigate whether dihydromyricetin modulates endothelial mitophagy and inhibits NLRP3 inflammasome activation to alleviate atherogenesis, along with the specific mechanisms involved. Methods: Apolipoprotein E-deficient mice on a high-fat diet were administered daily oral gavages of dihydromyricetin for 14 weeks. Blood samples were procured to determine the serum lipid profiles and quantify proinflammatory cytokine concentrations. Aortas were harvested to evaluate atherosclerotic plaque formation and NLRP3 inflammasome activation. Concurrently, in human umbilical vein endothelial cells, Western blotting, flow cytometry, and quantitative real-time PCR were employed to elucidate the mechanistic role of mitophagy in the modulation of NLRP3 inflammasome activation by dihydromyricetin. Results: Dihydromyricetin administration significantly attenuated NLRP3 inflammasome activation and vascular inflammation in mice on a high-fat diet, thereby exerting a pronounced inhibitory effect on atherogenesis. Both in vivo and in vitro, dihydromyricetin treatment markedly enhanced mitophagy. This enhancement in mitophagy ameliorated the mitochondrial damage instigated by saturated fatty acids, thereby inhibiting the activation and nuclear translocation of NF-κB. Consequently, concomitant reductions in the transcript levels of NLRP3 and interleukin-1β (IL-1β), alongside decreased activation of NLRP3 inflammasome and IL-1β secretion, were discerned. Notably, the inhibitory effects of dihydromyricetin on the activation of NF-κB and subsequently the NLRP3 inflammasome were determined to be, at least in part, contingent upon its capacity to promote mitophagy. Conclusion: This study suggested that dihydromyricetin may function as a modulator to promote mitophagy, which in turn mitigates NF-κB activity and subsequent NLRP3 inflammasome activation, thereby conferring protection against atherosclerosis. [ABSTRACT FROM AUTHOR]

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Dihydromyricetin (DHM or DMY) is a flavonoid derived from natural sources with a range of confirmed biological benefits. It exhibits anti-inflammatory, antioxidant, anti-tumor, and anti-viral activities. DHM is recognized for its high biosafety, making it a promising subject for further research. This article offers a comprehensive overview of DHM’s pharmacological properties, mechanisms, and recent research developments in the cardiovascular, urinary, digestive, nervous, and respiratory systems. The review summarizes DHM’s biological effects and associated signaling pathways, providing novel insights for its clinical application.

Ischemic stroke (IS) remains a leading cause of disability and mortality worldwide, and inflammation and oxidative stress play significant roles in its pathogenesis. This study investigates the effects of dihydromyricetin (DHM) on IS using RT-qPCR and western blot with SH-SY5Y cells, focusing on its effects on the small nucleolar RNA host gene 10 (SNHG10)/microRNA (miR)-665/Ras association domain family member 5 (RASSF5) axis and nuclear factor-kappa B (NF-κB) signaling. In addition, the effects of the SNHG10/miR-665/RASSF5 axis on SH-SY5Y cell activity, apoptosis, oxidative stress, and inflammatory markers were analyzed using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, flow cytometry, and enzyme-linked immunosorbent assays. Our results showed that, in response to oxygen-glucose deprivation/reperfusion (OGD/R), DHM treatment improved cell viability, reduced apoptosis, and attenuated neuroinflammation and oxidative stress in a dose-dependent manner (p

Vine tea is a traditional Chinese tea that has been used for centuries. It is rich in flavonoids and has excellent health benefits, especially for liver. The aim of this study was to investigate the hepatoprotective mechanism of dihydromyricetin (DMY), a flavonoid mainly contained in vine tea. Six-week-old male C57BL/6J mice were administered different doses of DMY by oral gavage for two weeks. Liver function and physiological indices of mice were assessed, while changes in gut microbiota following DMY treatment were monitored through 16S rDNA gene sequencing. Additionally, metabolic pathways and mechanisms were further explored using RT-qPCR and Western blot analysis. The results showed that aspartate aminotransferase and alanine aminotransferase levels were significantly reduced after DMY intervention in mice. Meanwhile, the diversity and abundance of gut microbiota was increased by DMY. Moreover, DMY enhanced gut microbiota-mediated primary and secondary bile acid synthesis pathways. It inhibited the expression of bile acid synthesis rate-limiting enzymes, such as cyp7a1 and cyp27a1, in mouse liver tissue. However, bile acid-related receptors including fxr, FGFR4, and TGR5 were significantly activated, indicating that DMY inhibited bile acid synthesis in the liver. This negative feedback regulation mechanism, in which DMY participated, maintained bile acid homeostasis in the liver and intestine of mice. In conclusion, DMY modulated the composition of intestinal microbiota and its mediated bile acid homeostasis in mice, thereby exhibiting a protective effect on liver tissue.

Dihydromyricetin (DMY) has been encapsulated in delivery systems to address the solubility limitations of DMY in water and improve its bioavailability. Air-assisted electrospinning has been used as a novel technology to load DMY. To evaluate the impact of adding DMY to dextran/zein nanofibers and understand the effects of the Maillard reaction (MR) on the physical and functional properties of DMY-loaded nanofibers, dextran/zein/xylose nanofibers with 0%, 1%, 2%, 3%, and 4% DMY were fabricated, followed by MR crosslinking. Scanning electron microscopy (SEM) observations indicated that the addition of DMY and the MR did not affect the morphology of the nanofibers. X-ray diffraction (XRD) results indicated amorphous dispersion of DMY within the nanofibers and a decreased crystalline structure within the nanofibers following the MR, which might improve their molecular flexibility. The nanofibrous film formed after the MR exhibited both increased tensile strength and elastic modulus due to hydrogen bonding within the nanofibers and increased elongation at break attributed to the increased amorphization of the structure after crosslinking. The nanofibers were also found to exhibit improved heat stability after the MR. The antioxidant activity of the nanofibers indicated a dose-dependent effect of DMY on radical scavenging activity and reducing power. The maintenance of antioxidant activity of the nanofibers after the MR suggested heat stability of DMY during heat treatment. Overall, dextran/zein nanofibers with various DMY contents exhibited tunable physical properties and effective antioxidant activities, indicating that dextran/zein nanofibers offer a successful DMY delivery system, which can be further applied as an active package. [ABSTRACT FROM AUTHOR]

This study aims to investigate the impact of four key factors, namely, temperature, water source, metal ion, and pH, on the stability of molecular chirality of dihydromyricetin (DMY) and proposed effective strategies for configuration protection. The findings reveal that temperatures exceeding 80°C could accelerate the racemization process of DMY, with a significant increase in racemization observed at 100°C. In addition, DMY exhibited heightened stability in ultrapure water as compared to various water sources, including pure water‐1, pure water‐2, mineral water, and running water. Notably, the presence of Fe2+ displayed an inhibitory effect on the racemization of DMY, whereas Mg2+, Ca2+, and Mn2+ showed a substantial promotional effect. Additionally, acidic conditions (pH < 5.0) were found to be protective for maintaining the stability of DMY, whereas alkaline conditions (pH > 9.0) were observed to be detrimental. Meanwhile, we first identified the presence of another pair of DMY isomers in this work. [ABSTRACT FROM AUTHOR]

In clinical flap practice, there are a lot of studies being done on how to promote the survival of distal random flap necrosis in the hypoxic and ischemic state. As a traditional Chinese medicine, dihydromyricetin (DHM) is crucial in preventing oxidative stress and apoptosis in a number of disorders. In this work, we examined the impact of DHM on the ability to survive of ischemia flaps and looked into its fundamental mechanism. Our results showed that DHM significantly increased the ischemic flaps' survival area, encouraged angiogenesis and blood flow, reduced oxidative stress and apoptosis, and stimulated KEAP1‐Nrf2 (Kelch‐like ECH‐associated protein 1‐nuclear factor erythroid 2‐related factor) signaling pathways. Adeno‐associated virus (AAV) upregulation of KEAP1 expression also negated the favorable effects of DHM on flap survival. By activating KEAP1‐Nrf2 signaling pathways, DHM therapy promotes angiogenesis while reducing oxidative stress and apoptosis. [ABSTRACT FROM AUTHOR]

Cisplatin is a widely used chemotherapy drug for the treatment of various cancers. However, although cisplatin is effective in targeting cancer cells, it has severe side effects including skeletal muscle atrophy. In this study, we aimed to characterize the role of Dihydromyricetin in cisplatin-induced muscle atrophy in mice. 5-week-old male C57BL/6 mice were treated with Dihydromyricetin for 14 days orally followed by in intraperitoneally cisplatin administration for 6 days. Gastrocnemius muscles were isolated for the following experiments. Antioxidative stress were determined by peroxidative product malondialdehyde (MDA) and antioxidants superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities. Quadriceps muscle mass and grip strength were significantly restored by Dihydromyricetin in a dose-dependent manner. Moreover, muscle fibers were improved in Dihydromyricetin treated group. Excessive skeletal muscle E3 ubiquitin-protein ligases in cisplatin group were significantly repressed by Dihydromyricetin treatment. Dihydromyricetin significantly reduced oxidative stress induced by cisplatin by decreasing MDA level and restored SOD and GPx activities. In addition, ferroptosis was significantly reduced by Dihydromyricetin characterized by reduced iron level and ferritin heavy chain 1 and improved Gpx4 level. The present study demonstrated that Dihydromyricetin attenuated cisplatin-induced muscle atrophy by reducing skeletal muscle E3 ubiquitin-protein ligases, oxidative stress, and ferroptosis. [ABSTRACT FROM AUTHOR]

Intestinal fibrosis is a common complication of inflammatory bowel disease and is characterized by tissue stiffening and luminal narrowing. Dihydromyricetin (DHM) can alleviate liver fibrosis and renal interstitial fibrosis by inducing autophagy. However, whether DHM can alleviate intestinal fibrosis remains unclear. This study is aimed at evaluating the role and mechanism of action of DHM in inflammatory bowel disease-associated intestinal fibrosis. Mice were administered dextran sulfate sodium (DSS) in drinking water to induce inflammatory bowel disease-associated intestinal fibrosis. HE staining, qPCR, and Western blotting were used to analyze colon inflammation. Masson's trichrome staining, qPCR, Western blotting, and immunofluorescence staining were used to evaluate the severity of fibrosis. Transmission electron microscopy and Western blotting were used to assess the activation of autophagosomes. The human colonic fibroblast line CCD-18Co was cultured in the presence of TGF-β1 to develop a fibrotic phenotype. Immunofluorescence staining, Western blotting, and qPCR were used to assess the alteration of fibrosis markers and used to investigate whether DHM-induced autophagy was involved in the inactivation of CCD-18Co cells. Additionally, the role of the PI3K/AKT/mTOR pathway was investigated. DHM alleviated intestinal inflammation and inhibited the progression of intestinal fibrosis. Additionally, DHM induced the activation of autophagy, thereby alleviating intestinal fibrosis, and downregulated the PI3K/AKT/mTOR signaling pathway in vitro. Overall, this study demonstrated that DHM can inhibit the progression of intestinal fibrosis and activation of colonic fibroblasts by inducing autophagy through the PI3K/AKT/mTOR signaling pathway, thereby playing a preventive and therapeutic role in intestinal fibrosis. [ABSTRACT FROM AUTHOR]

[Objective] To study the processing technology of Hovenia dulcis juice and the determination method of dihydromyricetin content in the juice. [Method] A single factor experiment was used to screen the processing technology of Hovenia dulcis juice, and the decoction method and extraction method were compared. The crushing particle size, water addition amount and soaking time were examined. The determination method of dihydromyricetin content in Hovenia dulcis juice was established and methodological studies were conducted. [Result] The Hovenia dulcis juice obtained by the extraction method had a good taste, with the crushing particle size of 8 mesh sieves, the water addition amount of 1.3-1.5 times and the soaking time of 18 hours. The determination method for dihydromyricetin content was as follows: chromatographic column was Ajilent HC-C18, mobile phase was 0.1% phosphoric acid solution: acetonitrile 18: 82, flow rate was 1 mL/min, detection wavelength was 290 nm, column temperature was 30 °C, injection amount was 10 µL. [ Conclusion] The juice processing technology is simple and feasible, the juice has a good taste and is easy to achieve industrial production. The determination method of dihydromyricetin content has high accuracy, precision and specificity, this provides a basis for the formulation of quality standards for Hovenia dulcis juice. [ABSTRACT FROM AUTHOR]

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Background: In modern diets, alcohol consumption has led to an increase in the number of cases of alcohol-related liver disease (ALD). Dihydromyricetin (DMY) is commonly used as a hepatoprotective agent owing to its remarkable efficacy in treating chronic alcoholic liver injury; however, its mechanism of action is unclear. The object of the study is to investigate the effect and mechanism of DMY in alleviating chronic ALD. Methods: A mouse model of chronic ALD was established. Mice were treated with DMY for 56 days, and their biochemical parameters including liver function, blood lipids, and oxidative stress-related indices were measured. Farnesoid X receptor (FXR) expression, NOD-like receptor protein 3 (NLRP3) pathway-related protein expression, and inflammation-related gene expression were determined to elucidate the mechanism of DMY in mice with ALD. Lastly, serum and liver metabolomics-based UHPLC-Orbitrap Exploris MS analyses were used to determine the influence of the metabolism of DMY on mice with ALD. Results: Pharmacodynamic studies showed that DMY could decrease aspartate transaminase, alanine transaminase, triglyceride, and low-density lipoprotein cholesterol levels, improve superoxide dismutase activity, and reduce inflammation in mice with ALD. DMY treatment protects the liver by increasing FXR protein expression and by decreasing NLRP3 pathway-related protein expression and inflammatory gene expression. Metabolomics analysis indicated that ethanol treatment mainly altered metabolism in mice. DMY could regulate 10 metabolites in serum, namely, N-α-acetyllysine, 1-pyrrolinecytosine, glutamyllysine, 5-methylcytosine, N-methylvaline, pyridoxamine, demethoxycurcumin, L-arginine, triacetin, and 15-methylpalmitate. It could also regulate 31 metabolites in the liver, including L-methionine and L-leucine. DMY treatment altered the following important pathways: valine, leucine, and isoleucine biosynthesis; cysteine and methionine metabolism; and valine, leucine, and isoleucine degradation. Correlation analyses using heatmaps revealed that the metabolic parameters are closely related to the pharmacodynamic index. Conclusion: These findings indicated that DMY alleviated ALD by regulating the FXR-NLRP3 signaling pathway and could treat serum and liver metabolic disorders. [ABSTRACT FROM AUTHOR]

Diabetic wound is one of the serious complications of diabetes, and the wound is persistent and easily recurring, which seriously endangers the health and life of patients. How to effectively promote the healing of diabetic wounds has been a hot spot and difficult area of clinical research. Some previous studies have shown that dihydromyricetin has the effects of regulating blood glucose, controlling the severity, and inhibiting scarring. In the present study, we used polylactic-co-glycolic acid nanoparticles as a carrier to load dihydromyricetin to make drug-loaded nanoparticles and applied them dropwise (200 µL) to diabetic mice wounds by topical application to observe the healing and scar formation of diabetic wounds. We found that the healing rate of the diabetic mice was faster and the scar formation was less obvious. In addition, the elevated blood glucose level and weight loss of the mice in the treatment group were also reduced. Therefore, nanoparticle-mediated dihydromyricetin may be an effective treatment for diabetic wounds. [ABSTRACT FROM AUTHOR]