CARBOHYDRATE POLYMERS
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2014
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IF 3.916
Yashu Yao,Yan Xie,Chao Hong,Guowen Li,Hongyi Shen,Guang Ji
Myricetin shows low oral bioavailability (<10%) in rats due to poor aqueous solubility, though it has various pharmacological activities. Complexation with cyclodextrins (CDs) is a potent pharmaceutical method to enhance the bioavailability of poorly soluble compounds. The myricetin/HP-β-CD inclusion complex was prepared and confirmed by DSC, PXRD, and SEM. Here, the inclusion mode is described in detail with regard to structural and energetic aspects using a phase solubility diagram and 1 H NMR, NOESY, and FT-IR spectra. The water solubility and dissolution rate of myricetin were greatly enhanced by forming the myricetin/HP-β-CD inclusion complex. Consequently, the oral bioavailability of the myricetin/HP-β-CD inclusion complex in rats was effectively increased 9.4-fold over free myricetin, and its antioxidant activity was also improved. The present study provides useful information for the potential application of complexation with myricetin, a naturally occurring hydrophobic phenolic compound in herbal medicine.
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NUTRITION RESEARCH
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2015
·
IF 2.472
Qian Wang,Shuang-ting Wang,Xin Yang,Pan-pan You,Wen Zhang
Myricetin (MyR), a naturally occurring flavonol widely distributed in fruits, vegetables, and medicinal plants , has anticancer, anti-inflammatory, antihyperlipidaemic , and antiobesity activities. In the present study, we hypothesized that the antiobesity property of MyR is mediated via suppression of differentiation of preadipocytes into adipocytes and promotion of lipolysis of mature adipocytes, which effectively decrease the intracellular triglyceride concentration of adipocytes. Accordingly, the aim of this work was to investigate the effects of MyR on adipocyte differentiation and lipolysis in differentiated 3 T3-L1 adipocytes. Our results showed that MyR inhibited differentiation of 3 T3-L1 preadipocytes in a concentration-dependent manner. Myricetin downregulated the mRNA and protein levels of CCAAT/enhancer-binding protein α and peroxisome proliferator-activated receptor γ , both of which are major adipogenic transcription factors. Furthermore, the mRNA levels of other adipogenesis-related transcription factors, namely, CCAAT/enhancer-binding protein β , sterin regulatory element binding protein 1-c, peroxisome proliferator-activated receptor γ coactivator–1, adipocyte protein 2 , lipoprotein lipase and glucose transporter 4 , were also reduced by MyR treatment. Moreover, MyR significantly inhibited the phosphorylation of extracellular signal–regulated kinase, Jun N-terminal kinase, and p38 during the differentiation process. On the other hand, MyR induced a dose-dependent increase in glycerol release in fully differentiated adipocytes, indicating its stimulatory effect on adipocyte lipolysis. Furthermore, MyR downregulated mRNA level of perilipin A and enhanced the phosphorylation level of extracellular signal–regulated kinase, Jun N-terminal kinase, and p38 during lipolysis. Taken together, these findings indicate that MyR exerts antiobesity activity in adipocytes.
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FOOD CHEMISTRY
·
2025
·
IF 9.8
Shengxiong Chen,Fan Zhang,Aline Priscilla Gomes da Silva,Jesus Simal-Gandara,Hui Cao
Myricetin, a bioactive flavonoid, degrades rapidly in boiling water, limiting its use in functional foods and pharmaceuticals. This study explores the protective effect of vitamin C on the thermal degradation of myricetin and its mechanism of action. O -phenylenediamine derivatization identified reactive ortho-quinone intermediates, while density functional theory (DFT) calculations (ΔG = −47.74 kcal/mol) confirmed the redox mechanism. Vitamin C significantly improved myricetin retention from 32.8 % to 91.4 % in 0.8 mM after 100 min of heating, outperforming nitrogen treatment. Myricetin degradation begins with oxidation to ortho-quinones, which further degrades into phenolic acids and aldehydes. Vitamin C not only inhibited this process but also reversed oxidation by reducing ortho-quinones back to myricetin. These findings highlight vitamin C's potential to enhance flavonoid stability and bioavailability in functional heat-processed foods.
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MOLECULES
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2024
·Vol. 29
·期 10
·2354
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IF 4.2
Jia-Le Zhou,Hao-Han Chen,Jian Xu,Ming-Yu Huang,Jun-Feng Wang,Hao-Jie Shen,Sheng-Xiang Shen,Cheng-Xian Gao,Chao-Dong Qian
Background:Staphylococcus aureusis a common pathogenic microorganism in humans and animals. Type II NADH oxidoreductase (NDH-2) is the only NADH:quinone oxidoreductase present in this organism and represents a promising target for the development of anti-staphylococcal drugs. Recently, myricetin, a natural flavonoid from vegetables and fruits, was found to be a potential inhibitor of NDH-2 ofS. aureus. The objective of this study was to evaluate the inhibitory properties of myricetin against NDH-2 and its impact on the growth and expression of virulence factors inS. aureus. Results: A screening method was established to identify effective inhibitors of NDH-2, based on heterologously expressedS. aureusNDH-2. Myricetin was found to be an effective inhibitor of NDH-2 with a half maximal inhibitory concentration (IC50) of 2 μM. In silico predictions and enzyme inhibition kinetics further characterized myricetin as a competitive inhibitor of NDH-2 with respect to the substrate menadione (MK). The minimum inhibitory concentrations (MICs) of myricetin againstS. aureusstrains ranged from 64 to 128 μg/mL. Time–kill assays showed that myricetin was a bactericidal agent againstS. aureus. In line with being a competitive inhibitor of the NDH-2 substrate MK, the anti-staphylococcal activity of myricetin was antagonized by MK-4. In addition, myricetin was found to inhibit the gene expression of enterotoxin SeA and reduce the hemolytic activity induced byS. aureusculture on rabbit erythrocytes in a dose-dependent manner. Conclusions: Myricetin was newly discovered to be a competitive inhibitor ofS. aureusNDH-2 in relation to the substrate MK. This discovery offers a fresh perspective on the anti-staphylococcal activity of myricetin.
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Nutrients
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2016
·Vol. 8
·期 12
·799
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IF 3.759
Shu-Fang Xia,Guo-Wei Le,Peng Wang,Yu-Yu Qiu,Yu-Yu Jiang,Xue Tang
Myricetin is an effective antioxidant in the treatment of obesity and obesity-related metabolic disorders. The objective of this study was to explore the regressive effect of myricetin on pre-existing hepatic steatosis induced by high-fat diet (HFD). C57BL/6 mice were fed either a standard diet or a HFD for 12 weeks and then half of the mice were treated with myricetin (0.12% in the diet,w/w) while on their respective diets for further 12 weeks. Myricetin treatment significantly alleviated HFD-induced steatosis, decreased hepatic lipid accumulation and thiobarbituric acid reactive substance (TBARS) levels, and increased antioxidative enzyme activities, including catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GPx) activities. Microarray analysis of hepatic gene expression profiles showed that myricetin significantly altered the expression profiles of 177 genes which were involved in 12 biological pathways, including the peroxisome proliferator activated receptor (PPAR) signaling pathway and peroxisome. Further research indicated that myricetin elevated hepatic nuclear Nrf2 translocation, increased the protein expression of heme oxygenase-1 (HO-1) and NAD(P)H quinone dehydrogenase 1 (NQO1), reduced the protein expression of PPARγ, and normalized the expressions of genes that were involved in peroxisome and the PPAR signaling pathway. Our data indicated that myricetin might represent an effective therapeutic agent to treat HFD-induced hepatic steatosis via activating the Nrf2 pathway and the PPAR signaling pathway.Keywords:myricetin;hepatic steatosis;Nrf2;PPARγ;oxidative stress
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JOURNAL OF CHROMATOGRAPHY B-ANALYTICAL TECHNOLOGIES IN THE BIOMEDICAL AND LIFE SCIENCES
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2013
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IF 2.487
Shian Zhong,Yanyue Kong,Ling Zhou,Chengyun Zhou,Xiaona Zhang,Yan Wang
In this study, we developed an efficient conversion process of dihydromyricetin to myricetin from Ampelopsis grossedentata extracts. The content of myricetin increased from 2.38% to 85.57%, demonstrating the successful dehydrogenation of dihydromyricetin. Molecularly imprinted polymers (MIPs) were prepared by surface imprinting method using silica microspheres as the support matrices and myricetin as template. The MIPs were applied for the selective adsorption of myricetin. The chemical structure of the MIPs was characterized by Fourier transform infrared spectroscopy and scanning electron microscopy. Static, dynamic and selective adsorption experiments showed that the MIPs exhibited good adsorption ability, rather fast template rebinding kinetics, and appreciate selectivity over structurally related compounds. Accordingly, the MIPs were applied as the selective sorbent in SPE to purify myricetin obtained through dehydrogenation, followed by HPLC-UV analysis. The recoveries of myricetin and dihydromyricetin were 92.7% and 55.6%, respectively. This study demonstrates the feasibility of using the developed MIP-SPE method to purify and enrich myricetin in the natural products.
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FOOD CHEMISTRY
·
2024
·
IF 8.5
Lei Xie,Tianxing Wang,Ling Chen,Xiaoxi Li
This study aims to investigate the inhibition of myricetin on heterocyclic aromatic amines (HAAs) formation in glucose/creatine (creatinine)/amino acid simulated system and Cantonese mooncakes, and elucidate the mechanism by which myricetin inhibits HAAs and analyze its impact on sensory quality of mooncakes. Results demonstrated 0.2 mmol myricetin inhibited six HAAs by 43.7 % to 85.6 % in simulated system. The significant scavenging effect of myricetin on HAAs intermediates and free radicals suggested that it inhibits HAAs formation by forming adducts with Strecker aldehydes, thereby reducing small molecule aldehydes and scavenging free radicals. In Cantonese mooncakes, 0.5 % myricetin inhibited nine HAAs formation by 54.4 % to 81.8 %. The presence of myricetin-phenylacetaldehyde adducts confirmed myricetin inhibited HAAs formation by capturing reactive intermediates. Importantly, 0.2 % myricetin enhanced umami and richness without compromising their texture in mooncakes. This research provides a theoretical foundation and technical support for developing strategies to effectively inhibit HAAs generation, thus advancing food safety.
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BIOMEDICINE & PHARMACOTHERAPY
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2024
·
IF 6.9
Jaili Li,Ting Luo,Yao Zhao,Dou Wang,Yuanxiang Jin,Zufang Wu,Guiling Yang,Xingjiang Qi
Doxorubicin (DOX) is a commonly used anthracycline in cancer chemotherapy. The clinical application of DOX is constrained by its cardiotoxicity. Myricetin (MYR) is a natural flavonoid widely present in many plants with antioxidant and anti-inflammatory properties. However, MYR's beneficial effects and mechanisms in alleviating DOX-induced cardiotoxicity (DIC) remain unknown. C57BL/6 mice were injected with 15 mg/kg of DOX to establish the DIC, and MYR solutions were administrated by gavage to investigate its cardioprotective potentials. Histopathological analysis, physiological indicators assessment, transcriptomics analysis, and RT-qPCR were used to elucidate the potential mechanism of MYR in DIC treatment. MYR reduced cardiac injury produced by DOX, decreased levels of cTnI, AST, LDH, and BNP, and improved myocardial injury and fibrosis. MYR effectively prevented DOX-induced oxidative stress, such as lowered MDA levels and elevated SOD, CAT, and GSH activities. MYR effectively suppressed NLRP3 and ASC gene expression levels to inhibit pyroptosis while regulating Caspase1 and Bax levels to reduce cardiac cell apoptosis. According to the transcriptomic analysis, glucose and fatty acid metabolism were associated with differential gene expression. KEGG pathway analysis revealed differential gene enrichment in PPAR and AMPK pathways, among others. Following validation, MYR was found to alleviate DIC by regulating glycolipid metabolism and AMPK pathway-related genes. Our findings demonstrated that MYR could mitigate DIC by regulating the processes of oxidative stress, apoptosis, and pyroptosis. MYR is critical in improving DOX-induced myocardial energy metabolism abnormalities mediated by the AMPK signaling pathway. In conclusion, MYR holds promise as a therapeutic strategy for DIC.
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MICROCHEMICAL JOURNAL
·
2026
·
IF 5.2
Rui Cheng,Hongan Zhang,Ziqi He,Xueting Luo,Wanju Zhang,Ziqiang Xu,Minsong Lin
Myricetin-derived carbon dots enable ratio-metric pH sensing with pH from 7.2 to 9.6. • Hydrazone structures confer highly sensitive and selective Al 3+ recognition. • Confocal imaging validates dual-function intracellular pH and Al 3+ monitoring. Sensitive analysis of intracellular pH and Al 3+ is essential for biological and environmental accessment. And traditional fluorescent nanomaterials often contain heavy metal components, whereas carbon dots (CDs) are metal-free with excellent biocompatibility, making them attractive candidates for probe construction. However, most CDs-based fluorescent probes have been developed empirically, with rational design strategies remaining relatively limited. Therefore, hydrazone functionalized carbon dots (N 2 H 4 @CDs) are fabricated by combining natural myricetin precursor with hydrazine-assisted post-functionalization strategy, establishing a structure-guided design that enables both ratio-metric pH sensing and selective Al 3+ analysis. Notably, N 2 H 4 @CDs showed dual emissions at 495 and 570 nm, with the peak at 570 nm increasing under higher pH. This ratio-metric response enabled accurate self-calibrated analyzing, showing a great linear correlation between the ratio I 495 / I 570 and pH from 7.2 to 9.6. As for Al 3+ analysis, fluorescence spectra show a pronounced enhancement of the emission intensity at 495 nm upon addition of Al 3+ , reflecting specific coordination with surface functional groups. The N 2 H 4 @CDs platform enable sensitive analysis of Al 3+ , with a linear range of 2–18 μmol/L and a detection limit of 0.125 μmol/L (3.37 μg/L). The spiked recovery experiments in lake water yielded satisfactory results, indicating its potential application in environmental exposure analysis. Confocal imaging in L929 fibroblasts confirmed that N 2 H 4 @CDs enable imaging of intracellular pH and Al 3+ . This strategy propses a rational hydrazone engineering strategy to realize ratiometric pH imaging as well as selective Al 3+ sensing. Download: Download high-res image (100KB) Download: Download full-size image
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TOXICOLOGICAL SCIENCES
·
2022
·Vol. 191
·期 2
·308-320
·
IF 4.109
Gao Jie-Fang,Tang Liu,Luo Fei,Chen Lu,Zhang Yi-Yuan,Ding Hong
Atopic dermatitis (AD) is a chronic, inflammatory cutaneous disorder. Obesity is associated with increased prevalence and severity of AD for reasons that remain poorly understood. Myricetin, a dietary flavonoid found in fruits and vegetables, is known to have anti-inflammatory effects, but its role in AD is unclear. Thus, we investigated the effects of obesity on exacerbation AD lesions and evaluated the effects of myricetin on obese AD. Mice were fed normal diet (ND) or high-fat diet, and then 2,4-dinitrofluorobenzene was used to induce AD-like lesions. We found that obesity exacerbated AD lesions, and myricetin topical administration ameliorated symptoms and skin lesions of obsess AD mice, such as dermatitis scores, scratching behavior, epidermal thickness, and mast cell infiltration. In addition, myricetin reduced the levels of immunoglobulin E and histamine, inhibited the infiltration of CD4+T cells, and modulated the expression of Th1, Th2, Th17, and Th22 cytokines and pro-inflammatory factors (CCL17, CCL22, IL-1β, and TGF-β). Moreover, myricetin restored impaired barrier function by reducing transepidermal water loss, increasing lamellar body secretion, as well as upregulating the mRNA and protein expression of filaggrin. Western blot results showed that significantly increased levels of phosphorylated IκB and NF-κB p65 was observed in the obese AD mice compared with the AD mice fed ND, whereas the myricetin could downregulated the phosphorylations of IκB and NF-κB, and inhibited mRNA expression of iNOS and COX2. Taken together, our results suggest that myricetin treatment exhibits potentially protective effects against the obeseassociated AD by inhibiting inflammatory response and restoring skin barrier function.
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EUROPEAN JOURNAL OF NUTRITION
·
2017
·Vol. 57
·期 1
·391-403
·
IF 4.37
Hu Tao,Yuan Xiaoxue,Wei Gang,Luo Haoshu,Lee Hyuek Jong,Jin Wanzhu
Purpose Myricetin, a dietary flavonoid, is effective in the treatment of obesity and insulin resistance by increasing glucose transport and lipogenesis in adipocyte and diminishing systemic inflammation in obesity. However, it has not been revealed yet whether myricetin is associated with brown adipose tissue (BAT) activation that tightly mediates systemic energy metabolism. Therefore, this study assessed whether myricetin activated brown adipose tissue in db/db mouse. Methods Myricetin (400 mg/kg) in distilled water was fed daily by oral gavage to leptin receptor-deficient db/db male mice at 4 weeks of age for 14 weeks. Body weight change, glucose intolerance test, blood lipid profile and BAT activation using PET-CT were assessed. Results After myricetin treatment for 14 weeks, systemic insulin resistance and hepatic steatosis were significantly improved in db/db mice with body weight reduction and myricetin led to decreased adipocity, improved plasma lipid profiles and increased energy expenditure. Myricetin activated BAT by upregulating thermogenic protein expression and activating mitochondrial biogenesis, eventually increasing heat dissipation in skin after cold exposure. In iWAT, myricetin induced beige formation, increased thermogenic protein expression and activated mitochondrial biogenesis. Consistently, thermogenic gene expression was upregulated when myricetin was introduced in C 3 H 10 T 1/2 cells during brown adipocytes differentiation. Moreover, the expression level of adiponectin was significantly increased in C 3 H 10 T 1/2 cells, adipose tissues and plasma after myricetin treatment. Conclusions These results highlight that myricetin prevents obesity and systemic insulin resistance by activating BAT and increasing adiponectin expression in BAT.
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Scientific Reports
·
2024
·
IF 3.8
Si-Chun Gu,Zhi-Guo Xie,Min-Jue Gu,Chang-De Wang,Li-Min Xu,Chen Gao,Xiao-Lei Yuan,You Wu,Yu-Qing Hu,Yang Cao,Qing Ye
Ferroptosis is an iron-dependent cell death form characterized by reactive oxygen species (ROS) overgeneration and lipid peroxidation. Myricetin, a flavonoid that exists in numerous plants, exhibits potent antioxidant capacity. Given that iron accumulation and ROS-provoked dopaminergic neuron death are the two main pathological hallmarks of Parkinson’s disease (PD), we aimed to investigate whether myricetin decreases neuronal death through suppressing ferroptosis. The PD models were established by intraperitoneally injecting 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) into rats and by treating SH-SY5Y cells with 1-methyl-4-phenylpyridinium (MPP + ), respectively. Ferroptosis was identified by assessing the levels of Fe 2+ , ROS, malondialdehyde (MDA), and glutathione (GSH). The results demonstrated that myricetin treatment effectively mitigated MPTP-triggered motor impairment, dopamine neuronal death, and α-synuclein (α-Syn) accumulation in PD models. Myricetin also alleviated MPTP-induced ferroptosis, as evidenced by decreased levels of Fe 2+ , ROS, and MDA and increased levels of GSH in the substantia nigra (SN) and serum in PD models. All these changes were reversed by erastin, a ferroptosis activator. In vitro, myricetin treatment restored SH-SY5Y cell viability and alleviated MPP + -induced SH-SY5Y cell ferroptosis. Mechanistically, myricetin accelerated nuclear translocation of nuclear factor E2-related factor 2 (Nrf2) and subsequent glutathione peroxidase 4 (Gpx4) expression in MPP + -treated SH-SY5Y cells, two critical inhibitors of ferroptosis. Collectively, these data demonstrate that myricetin may be a potential agent for decreasing dopaminergic neuron death by inhibiting ferroptosis in PD.
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