• YAKHAK HOEJI
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• v.50 no.1
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• pp.58-63
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• 2006

The antioxidant enzyme (AOE) system plays an important role in the defense against oxidative stress damage. To determine whether myricetin or myricetin/taurine can exert antioxidative effects not only by modulating the AOE system directly but also by scavenging free radical, we investigated the influence of the myricetin and taurine on cell viability ROS level, activities of different antioxidant enzyme, and the expression of different antioxidant enzyme. As results, the cell viability showed inhibition of the proliferation with treatment of 'myricetin' or 'myricetin with taruine', respectively, with dose-dependent manner. Compared to control, the treatment of 'myricetin' decreased activities and gene expressions of superoxide dismutase (SOD), and glutathione peroxidase (GPx). However, combined treatment of 'myricetin with taurine' increased activities and gene expressions of the SOD, GPx, and catalase (CAT). In addition, the combined treatment of 'myricetin with taurine' somewhat decreased ROS levels, compared to the treatment of 'myricetin'. In conclusion, our study provides that the combined treatment of different antioxidants can enhance antioxidant effects.

• Journal of Microbiology and Biotechnology
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• v.32 no.1
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• pp.37-45
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• 2022

The fungal cell wall and membrane are the principal targets of antifungals. Herein, we report that myricetin exerts antifungal activity against Candida albicans by damaging the cell wall integrity and notably enhancing the membrane permeability. In the presence of sorbitol, an osmotic protectant, the minimum inhibitory concentration (MIC) of myricetin against C. albicans increased from 20 to 40 and 80 ㎍/ml in 24 and 72 h, respectively, demonstrating that myricetin disturbs the cell wall integrity of C. albicans. Fluorescence microscopic images showed the presence of propidium iodide-stained C. albicans cells, indicating the myricetin-induced initial damage of the cell membrane. The effects of myricetin on the membrane permeability of C. albicans cells were assessed using crystal violet-uptake and intracellular material-leakage assays. The percentage uptakes of crystal violet for myricetin-treated C. albicans cells at 1×, 2×, and 4× the MIC of myricetin were 36.5, 60.6, and 79.4%, respectively, while those for DMSO-treated C. albicans cells were 28.2, 28.9, and 29.7%, respectively. Additionally, myricetin-treated C. albicans cells showed notable DNA and protein leakage, compared with the DMSO-treated controls. Furthermore, treatment of C. albicans cells with 1× the MIC of myricetin showed a 17.2 and 28.0% reduction in the binding of the lipophilic probes diphenylhexatriene and Nile red, respectively, indicating that myricetin alters the lipid components or order in the C. albicans cell membrane, leading to increased membrane permeability. Therefore, these data will provide insights into the pharmacological worth of myricetin as a prospective antifungal for treating C. albicans infections.

• Journal of Physiology & Pathology in Korean Medicine
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• v.24 no.1
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• pp.74-79
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• 2010

Osteoclasts are bone-resorbing giant cells that differentiate from hematopoietic cells of the monocyte/macrophages. Excessive osteoclast differentiation leads to gradual loss of bone mass causing fracture of the skeleton. The aim of this study was to develop a drug candidates for the treatment of osteoporosis. RANKL-induced osteoclast differentiation was dose-dependently inhibited by myricetin. Myricetin inhibited the expression of c-Fos, NFATc1, and TRAP in BMMs treated with RANKL. Myricetin disrupted the structure of actin ring and suppressed osteoclastic bone resorption. Also, myricetin induced apoptosis in mature osteoclasts. Myricetin inhibited the phosphorylation of ERK in mature osteoclasts treated with M-CSF. The activation of caspase-9 and caspase-3 was increased by myricetin treatment. Our results suggest that myricetin may be an effective agent to prevent bone diseases such as osteoporosis.

• YAKHAK HOEJI
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• v.49 no.1
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• pp.86-91
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• 2005

Flavonoids are class of polyphenolic compounds widely distributed in the plant kingdom, which display a variety of biological activities, including antiviral, antithrombotic, antiinflammatory, antihistaminic, antioxidant and free-radica 1 scavenging abilities. The antioxidant enzyme (AOE) system plays an important role in the defense against oxidative stress insults. To determine whether flavonoid, myricetin can exert antioxidative effects not only directly by modulating the AOE system but also scavenging free radical, we investigated the influence of the flavonoid myricetin on cell viability, different antioxidant enzyme activities, ROS level and the expression of different antioxidant emzyme in B16F10 murine melanoma cells. Myricetin in a concentration range from 6.25 to $50\;{\mu}M$ decreased superoxide dismutase (SOD) and glutathione peroxidase (GPx) enzyme activities, but catalase (CAT) activity was increased. In the myricetin-treated group, ROS levels were decreased dose-dependently. Antioxidant enzyme expression was measured by RT-PCR. Myricetin treatment of B16F10 cells increased catalase expression. Expression levels of copper zinc superoxide dismutase (CuZn SOD) were not affected by exposure of myricetin. Manganese superoxide dismutase (Mn SOD) and GPx expression levels decreased slightly after myricetin treatment. In conclusion, the antioxidant capacity of myricetin was due to CAT and free-radical scavenging.

• International Journal of Oral Biology
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• v.41 no.4
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• pp.163-173
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• 2016

Flavonoid myricetin, usually found in tea and medicinal plants, has antioxidant and anti-inflammatory effects. Our objectives in this study were to verify the effects of myricetin on periodontal ligament fibroblasts (PDLFs) under inflammatory conditions and to observe its effects on osteoclast generation and on cytokine expression in RAW264.7 cells. To determine the effects of myricetin on PDLFs, we examined the expression and activity of proteolytic enzymes, including MMP-1, MMP-2, and MMP-8, which all play an important role in chronic periodontitis. We observed the effects of myricetin on intracellular signal transduction to verify the molecular mechanism involved. By measuring the formation of TRAP-positive multinucleated cells and the expression and activity of MMP-8, we were able to assess the effects of myricetin on osteoclast generation. In addition, by measuring the secretion of IL-6 and NO, we could evaluate the effects of myricetin on inflammatory mediators. We found that Myricetin had no effect on the viability of the PDLFs in the presence of inflammation, but it did decrease both the expression of MMP-1 and MMP-8 and the enzyme activity of MMP-2 and MMP-8 in these fibroblasts. Myricetin also decreased the lipopolysaccharide-stimulated phosphorylation of JNK, p38 signaling, IKKB, AKT, and p65RelA in the PDLFs. In the RAW264.7 cells, myricetin inhibited both the expression and the activity of MMP-8. Furthermore, Myricetin not only suppressed the generation of LPS-stimulated osteoclasts, but it also slightly inhibited LPS-stimulated degradation of IkB and decreased the release of LPS-induced IL-6 and NO. These findings suggest that myricetin alleviates the tissue-destructive processes that occur during periodontal inflammation.

• Journal of Physiology & Pathology in Korean Medicine
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• v.18 no.3
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• pp.830-836
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• 2004

The unique biochemical pathways in melanocytes responsible for melanogenesis provide us with a rational mechanism-based means for developing both pharmacological regulators of pigmentation and cytotoxic chemotherapeutic drugs for melanoma, Myricetin is a polyphenolic antioxidant and a component from Biotae Semen, Biotae orientalis Folium. Therefore, the present study was conducted to evaluate the effects of myricetin on the melanogenesis in human melanoma (HM₃KO) cells. The cells were treated for 5 days with myricetin at several concentrations (10 - 100 μg/ml). Treatment with myricetin dose-dependently suppressed cell growth in HM₃KO cells, But melanin formation was markedly increased by myricetin as a dose dependent manner. Myricetin did not affect to tyrosinase activity, which is a key enzyme for melanogenesis, but significantly increased the level of tyrosinase protein expression, These results suggest that myricetin stimulate melanin synthesis of human melanoma cells through the modification of tyrosinase protein expression.

• Korean Journal of Pharmacognosy
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• v.35 no.4 s.139
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• pp.357-363
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• 2004

Flavonoids are class of polyphenolic compounds widely distributed in the plant kingdom, which display a variety of biological activities, including antiviral, antithrombotic, antiiflammatory, antihistaminic, antioxidant and free-radical scavenging abilities. To determined flavonoid, myricetin in the presence of other antioxidants - vitamin C and vitamin E - can exert antioxidative properties not only directly by modulating the AOE system but also scavenging free radical, we investigated cell viability, antioxidant enzyme activities and ROS level in B16F10 murine melanoma cell. B16F10 cells were exposed to medium containing myricetin in the presence or absence of vitamin C or vitamin E for a period of 24 hr. Cell viability was measured by MTT assay. In co-treating myricetin with other antioxidants, CAT activities were increased, compared with control, but SOD and GPx activities were decreased, compared with each antioxidant treated groups . In the group of myricetin or myricetin present with other antioxidants, ROS levels were decreased dose-dependently. Especially, myricetin present of other antioxidants were decreased compared with myricetin.

• Bulletin of the Korean Chemical Society
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• v.29 no.8
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• pp.1505-1509
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• 2008

Comparative molecular simulations were performed to establish molecular interaction and inhibitory effect of flavonoid myricetin on formation of amyloid fibris. For computational comparison, the conformational stability of myricetin with amyloid $\beta$ -peptide (A$\beta$ ) and $\beta$ -amyloid fibrils (fA$\beta$) were traced with multiple molecular dynamics simulations (MD) using the CHARMM program from Monte Carlo docked structures. Simulations showed that the inhibition by myricetin involves binding of the flavonoid to fA$\beta$ rather than A$\beta$ . Even in MD simulations over 5 ns at 300 K, myricetin/fA$\beta$ complex remained stable in compact conformation for multiple trajectories. In contrast, myricetin/A$\beta$ complex mostly turned into the dissociated conformation during the MD simulations at 300 K. These multiple MD simulations provide a theoretical basis for the higher inhibitory effect of myricetin on fibrillogenesis of fA$\beta$ relative to A$\beta$ . Significant binding between myricetin and fA$\beta$ observed from the computational simulations clearly reflects the previous experimental results in which only fA$\beta$ had bound to the myricetin molecules.

• Nutrition Research and Practice
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• v.8 no.5
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• pp.544-549
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• 2014

BACKGROUND/OBJECTIVES: Obesity-associated insulin resistance is a strong risk factor for type 2 diabetes mellitus. The aim of this study was to investigate the effect of myricetin on adiposity, insulin resistance, and inflammatory markers in mice with diet-induced insulin resistance. MATERIALS/METHODS: Five-week-old male C57BL/6J mice were fed a basal diet, a high-fat, high-sucrose (HFHS) diet, or the HFHS diet containing 0.06% myricetin or 0.12% myricetin for 12 weeks after a 1-week adaptation, and body weight and food intake were monitored. After sacrifice, serum lipid profiles, glucose, insulin, adipocyte-derived hormones, and proinflammatory cytokines were measured. The homeostasis model assessment for insulin resistance (HOMA-IR) was determined. RESULTS: Myricetin given at 0.12% of the total diet significantly reduced body weight, weight gain, and epidydimal white adipose tissue weight, and improved hypertriglyceridemia and hypercholesterolemia without a significant influence on food intake in mice fed the HFHS diet. Serum glucose and insulin levels, as well as HOMA-IR values, decreased significantly by 0.12% myricetin supplementation in mice fed the HFHS diet. Myricetin given at 0.12% of the total diet significantly reduced serum levels of leptin, tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$) and interleukin-6 (IL-6) in mice fed the HFHS diet. CONCLUSIONS: These findings suggest that myricetin may have a protective effect against diet-induced obesity and insulin resistance in mice fed HFHS diet, and that alleviation of insulin resistance could partly occur by improving obesity and reducing serum proinflammatory cytokine levels.

• Journal of Life Science
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• v.30 no.12
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• pp.1101-1108
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• 2020

Tartary buckwheat is a grain with many flavonoids, such as rutin, quercetin, kaempferol, and myricetin. This study aimed to optimize extraction conditions to maximize the rutin, quercetin, and myricetin contents of tartary buckwheat sprout extracts using response surface methodology. A BoxBehnken design containing 15 experiments was employed to evaluate the effects of extraction conditions, such as temperature (X1, 50~70℃), extraction time (X2, 5~9 hr), and ethanol concentration (X3, 60~90%). The coefficients of determination (R2) for all the dependent variables (extraction temperature, extraction time, and extraction ethanol concentration) were determined to be over 0.95, indicating significance. The p-value of the model in lack of fit was over 0.1 than means, indicating that the model was well predicted. The optimal extraction conditions for rutin, quercetin, and myricetin contents were obtained at X1 = 51.03, X2 = 6.62, and X3 = 69.16, respectively. Under these optimal conditions, the predicted rutin, quercetin, and myricetin contents were 808.467 ㎍/ml, 193.296 ㎍/ml, and 37.360 ㎍/ml, respectively. For the validation of the model, ten experiments were performed and the experimental rutin and quercetin contents were measured at 802.84±8.49 ㎍/ml, 193.76±2.80 ㎍/ml, and 34.84±0.43 ㎍/ml, respectively. The experimental rutin and quercetin contents were similar to the predicted contents, but the experimental myricetin content was lower than predicted.