Roles and mechanisms of quercetin on cardiac arrhythmia: A review

Zhou, Yutong; Suo, Wendong; Zhang, Xinai; Lv, Jiayu; Liu, Zhiming

doi:10.1016/j.biopha.2022.113447

Cited by 29 publications

(16 citation statements)

References 204 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…For instance, quercetin intake reduces blood pressure and prevents atherosclerosis in hypertensive patients. 82 It also prevents heart failure by protecting the myocardial tissue through several mechanisms such as the inhibition of oxidative stress, 83 the elevation of SIRT5 (Sirtuin 5) expression in cardiac cells, 83 and the inhibition of PI3K/AKT and p53/p21/serpins pathways. 75 We found also evidence of quercetin reducing the risk of cardiac hypertrophy by inhibiting the proteasome and the activation of GSK3α (glycogen synthase kinase 3 alpha) and GSK3β (glycogen synthase kinase 3 beta) 84 and preventing ventricular arrhythmia in rats by inhibiting Na + inward flow and blocking ATXII (anemone toxin II)-induced late sodium currents.…”

Section: Predicted Mechanism Of Action For Amla’s Bioactive Small Mol...mentioning

confidence: 99%

“…75 We found also evidence of quercetin reducing the risk of cardiac hypertrophy by inhibiting the proteasome and the activation of GSK3α (glycogen synthase kinase 3 alpha) and GSK3β (glycogen synthase kinase 3 beta) 84 and preventing ventricular arrhythmia in rats by inhibiting Na + inward flow and blocking ATXII (anemone toxin II)-induced late sodium currents. 82 Similarly, Figure 2A illustrates how kaempferol is also proximal to hypertension, heart failure, arrhythmia, myocardial ischemia, pulmonary embolism, familial progressive cardiac conduction defect, and mitral valve prolapse. Evidence from the literature suggests that kaempferol exhibits cardioprotective effects, alleviates pulmonary arterial hypertension, and improves pulmonary vascular remodeling by downregulation of CYP2E1 (cytochrome P450 2E1), antioxidant activity, and inhibiting AKT/GSK3β and p38 MAPK kinase signaling pathways.…”

Section: Predicted Mechanism Of Action For Amla’s Bioactive Small Mol...mentioning

confidence: 99%

See 1 more Smart Citation

Molecular Interaction Networks and Cardiovascular Disease Risk: The Role of Food Bioactive Small Molecules

Nasirian

Menichetti

2023

ATVB

View full text Add to dashboard Cite

Diet is a well-known modifiable risk factor for cardiovascular diseases, which are the leading cause of death worldwide. However, our current understanding of the human diet is still limited in terms of fully capturing the role of dietary compounds in the intraspecies and interspecies biochemical networks that determine our health. This is due, in part, to a lack of detailed information on the presence of small molecules in food (molecular weight, ≤1000 daltons), their amounts, and their interactions with known protein targets. As a result, our ability to develop a mechanistic understanding of how food chemicals impact our health is limited. In recent years, the Foodome project has tackled several aspects of this challenging universe, leveraging the expertise of a diverse group of scientific communities, from computer science to epidemiology. Here, we review the most recent efforts of the Foodome project in mapping the chemical complexity of food and predicting its effect on human health. Leveraging the network medicine framework applied to Amla—a medicinal plant—we offer a rationale for future research on the mechanism of action of food bioactive small molecules, whose designing principles could inspire next-generation drug discovery and combinations.

show abstract

Section: Predicted Mechanism Of Action For Amla’s Bioactive Small Mol...mentioning

confidence: 99%

Section: Predicted Mechanism Of Action For Amla’s Bioactive Small Mol...mentioning

confidence: 99%

Molecular Interaction Networks and Cardiovascular Disease Risk: The Role of Food Bioactive Small Molecules

Nasirian

Menichetti

2023

ATVB

View full text Add to dashboard Cite

show abstract

“…Quercetin is widely present in many fruits and vegetables, especially in berries, apples, oranges, red grapes, tomatoes, buckwheat, onions, and broccoli [ 3 ]. Traditionally, quercetin has been used for the prevention and treatment of various diseases, such as diabetic nephropathy [ 4 ], neurological and neurodegenerative diseases [ 5 ], ischemic brain injury [ 6 ], and cardiovascular diseases [ 7 ]. Modern pharmacological research has shown that quercetin has multiple functions, such as reducing oxidative stress [ 8 ], reducing inflammation [ 9 ], protecting nerves [ 10 ], inhibiting platelet aggregation [ 11 ], relaxing vascular smooth muscle [ 12 ], and inhibiting cancer development [ 13 ].…”

Section: Introductionmentioning

confidence: 99%

Effects of quercetin on polycystic ovary syndrome in animal models: a systematic review and meta-analysis

Su,

Chen,

Pang

et al. 2024

Reprod Biol Endocrinol

View full text Add to dashboard Cite

Background Metformin is an insulin sensitizer that is widely used for the treatment of insulin resistance in polycystic ovary syndrome patients. However, metformin can cause gastrointestinal side effects. Purpose This study showed that the effects of quercetin are comparable to those of metformin. Therefore, this study aimed to systematically evaluate the efficacy of quercetin in treating PCOS. Methods The present systematic search of the Chinese National Knowledge Infrastructure (CNKI), Wanfang Data Information Site, Chinese Scientific Journals Database (VIP), SinoMed, Web of Science, and PubMed databases was performed from inception until February 2024. The methodological quality was then assessed by SYRCLE’s risk of bias tool, and the data were analyzed by RevMan 5.3 software. Results Ten studies were included in the meta-analysis. Compared with those in the model group, quercetin in the PCOS group had significant effects on reducing fasting insulin serum (FIS) levels (P = 0.0004), fasting blood glucose (FBG) levels (P = 0.01), HOMA-IR levels (P < 0.00001), cholesterol levels (P < 0.0001), triglyceride levels (P = 0.001), testosterone (T) levels (P < 0.00001), luteinizing hormone (LH) levels (P = 0.0003), the luteinizing hormone/follicle stimulating hormone (LH/FSH) ratio (P = 0.01), vascular endothelial growth factor (VEGF) levels (P < 0.00001), malondialdehyde (MDA) levels (P = 0.03), superoxide dismutase (SOD) levels (P = 0.01) and GLUT4 mRNA expression (P < 0.00001). Conclusion This meta-analysis suggested that quercetin has positive effects on PCOS treatment. Quercetin can systematically reduce insulin, blood glucose, cholesterol, and triglyceride levels in metabolic pathways. In the endocrine pathway, quercetin can regulate the function of the pituitary-ovarian axis, reduce testosterone and luteinizing hormone (LH) levels, and lower the ratio of LH to follicle-stimulating hormone (FSH). Quercetin can regulate the expression of the GLUT4 gene and has antioxidative effects at the molecular level.

show abstract

“…Quercetin, which is found in the seeds, flowers, bark, nuts and leaves of many plants, constitutes approximately 75% of the total flavonoid intake in the daily diet. Quercetin, which has anti-inflammatory, cardioprotective, antioxidant, anti-obesity, anti-mutagen, anti-diabetic, anti-hypercholesterolemic and anti-apoptotic activities, also draws attention with its anti-cancer properties 7 , 8 . There are many data on the protective properties of quercetin in the literature, but no study has been reported on its effect against AFM 2 toxicity.…”

Section: Introductionmentioning

confidence: 99%

Elucidating the toxicity mechanism of AFM2 and the protective role of quercetin in albino mice

Onur

Yalçın

Çavuşoğlu

et al. 2023

Sci Rep

View full text Add to dashboard Cite

Aflatoxin M2 (AFM2) is a type of mycotoxin detected in milk or dairy products from animals consuming contaminated feed. In this study, the toxicity mechanism of AFM2 and the protective effects of quercetin were investigated in albino mice. For this purpose, the mice were divided into 6 groups and the groups were fed with quercetin and AFM2. The toxic effects of AFM2 and the protective properties of quercetin were investigated using physiological, biochemical and cytogenetic parameters. The genotoxic mechanism of AFM2 and the protective role of quercetin were investigated by molecular docking, which is an in silico model. As a result, 16 mg/kg b.w AFM2 administration caused serious changes in body weight, organ index, kidney and liver weight, and deterioration of antioxidant/oxidant balance in liver and kidney organs. The decrease in glutathione levels along with an increase in malondialdehyde (MDA) levels in the liver and kidney after AFM2 administration indicates that oxidative stress is induced. The increases in alanine transaminase (ALT) and aspartat transaminase (AST) levels, which are indicators of liver damage, and the increases in serum levels of blood urea nitrogen (BUN) and creatinine, which are indicators of kidney damage, confirm the damage in both organs. AFM2 also caused genotoxicity by inducing micronucleus (MN) and chromosomal abnormalities (CAs) in bone marrow tissue. It has been determined that AFM2, which exhibits genotoxicity as a result of its clastogenic and aneugenic effects, causes CAs by interacting with DNA. Quercetin provided significant protection by improving liver and kidney tissues, partial normalization in serum parameter levels, and severe reductions in MN and CAs. The highest protection was determined as 74.1% against dicentric chromosome formations in 50 mg/kg b.w quercetin application. The interaction of quercetin with xanthine oxidase and nitric oxide synthase enzymes was determined in silico with an inhibition constant in the range of 283.71–476.17 nM. These interactions cause changes in the activity of enzymes, reducing the oxidative load in the cell, and in this way, quercetin provides protection. All toxic effects induced by AFM2 were decreased with quercetin administration dose-dependently, and this protective effect was associated with quercetin's reduction of oxidative load by inhibiting the free radical-producing enzyme. All toxic effects caused by AFM2 were decreased with quercetin administration in a dose-dependent manner, and this protective effect was associated with quercetin's reduction of oxidative load by inhibiting the enzyme that produces free radicals.

show abstract

Roles and mechanisms of quercetin on cardiac arrhythmia: A review

Cited by 29 publications

References 204 publications

Molecular Interaction Networks and Cardiovascular Disease Risk: The Role of Food Bioactive Small Molecules

Molecular Interaction Networks and Cardiovascular Disease Risk: The Role of Food Bioactive Small Molecules

Effects of quercetin on polycystic ovary syndrome in animal models: a systematic review and meta-analysis

Elucidating the toxicity mechanism of AFM2 and the protective role of quercetin in albino mice

Contact Info

Product

Resources

About