Humans cannot make quercetin in their bodies, but many fruits, vegetables, and drinks contain it. Foods and drinks that contain quercetin include :. Quercetin has antioxidant properties. Antioxidants help protect cells against oxidative damage.

The medical term for this is oxidative stress. Free radicals are unstable molecules in the body that can increase the risk of disease and quicken aging. The body produces free radicals through regular metabolic processes such as energy production.

Quercetin is a more powerful antioxidant than vitamin C, E , or beta carotene. However, chronic inflammation can harm the body and contribute to specific health conditions. Quercetin can help inhibit inflammation in the body.

While consuming a diet high in quercetin-rich foods may help regulate inflammation, it is unclear whether taking high dose quercetin supplements is beneficial for reducing inflammatory markers.

Research shows that a diet high in flavonoid-rich fruit and vegetables can lower the risk of certain cancers and slow cancer cell growth. However, more research is necessary to assess the direct links between quercetin intake and cancer risk.

Oxidative stress contributes to the development of neurodegenerative diseases. Oxidative stress occurs when there is an imbalance of free radicals in the body. The antioxidant properties of quercetin may help fight free radicals. A study found that consuming quercetin-rich onion for 24 weeks reduces age-related cognitive decline.

Additional findings from Pharmacognosy Review suggest that quercetin might be an effective antihistamine , as it restricts histamine from being released from cells. These anti-allergy properties indicate that quercetin may be a helpful supplement for those with allergic diseases, especially rhinitis.

However, more research is needed to confirm this potential benefit. People with allergies should not supplement with quercetin unless directed to do so by their healthcare professional. Quercetin has antibacterial and antiviral properties. Lab tests show that quercetin can inhibit the growth of many bacteria, including.

Quercetin, along with other flavonoids, may help inhibit the growth of many viruses. Diet plays an essential role in reducing the risk of cardiovascular diseases , such as heart disease and strokes.

Because fruit and vegetables contain flavonoids, eating more may help reduce the risk of these diseases. Research suggests that quercetin may help protect heart health by mitigating blood vessel dysfunction mitigating endothelial dysfunction, and reducing heart disease risk factors like high blood pressure and atherosclerosis.

According to a analysis , taking quercetin supplements could be an effective way to reduce blood pressure. Further research shows that people who were overweight and took a quercetin supplement of milligrams mg per day had lower levels of harmful cholesterol in their blood and reduced systolic blood pressure.

Systolic blood pressure measures the pressure in the blood vessels during a heartbeat. People can get quercetin through their diet by eating a range of fruit and vegetables daily. Onions are amongst the richest sources of dietary flavonoids you can eat, providing Quercetin is available as a nutritional supplement, typically in doses of to mg daily.

Supplements may also include other substances, such as bromelain or vitamin C, which may help the body absorb quercetin more effectively. The natural antioxidants found in fruits and vegetables can be beneficial when consumed as part of a balanced and nutritious diet. However, quercetin may interact with some medications, so people should ask their doctor before taking a supplement.

Quercetin is a flavonoid found in fruit and vegetables. It has a wide range of benefits, which people can get by including a variety of fruit and vegetables in their diet. Although many studies have found several potential benefits of quercetin, many have been animal or in vitro studies.

If people want to supplement their diet with quercetin, they should seek advice from a healthcare professional first. Free radicals are unstable atoms that can cause damage to cells and lead to illnesses and the aging process.

Exactly what impact do they have on the…. Canakinumab as an IL-1β neutralizing antibody, Anakinra as a recombinant human IL-1 receptor antagonist capable of inhibiting the binding of IL-1β and IL-1α, and rilonacept as IL-1 decoy receptor binding to IL-1β and IL-1α have been approved by the Food and Drug Administration FDA in the management of different inflammatory disorders [ 14 ].

However, IL-1β is only one of the proinflammatory cytokines involved in immunopathogenesis of diseases, which is itself the result of the activation of inflammation.

Directly targeting NLRP3 inflammasome is a much less invasive and more cost-effective method, and more specific than blocking cytokines. In vitro studies have shown that MCC can inhibit both focal and non-focal pathways of NLRP3 inflammasome activation in mice and human macrophages specifically without impairing the NLRP1, NLRC4 AIM2 inflammasome complexes, or without disrupting signaling pathways associated with Toll-like receptors TLRs.

A phase-II clinical trial that used MCC to treat rheumatoid arthritis was discontinued due to hepatotoxic effects. However, other studies have reported convincing reasons that have led future efforts to target NLRP3 inflammasome for the treatment of inflammatory diseases [ 20 ].

Drugs that have previously been approved by the US Food and Drug Administration or other human-used compounds that can effectively inhibit NLRP3 inflammasome could be a potential treatment in severe COVID cases. The thioredoxin interacting protein TXNIP gene is located on chromosome 1qq23 in the same locus as T2DM.

TXNIP is a central mediator that is associated with NLRP3 inflammasome activation by binding to NLRP3 as ROS-dependent manner after separation from Trx.

Inflammatory activators such as uric acid crystals cause the TXNIP to be separated from Trx by the ROS-sensitive method, thus facilitating the binding of TXNIP to NLRP3 [ 22 ].

TXNIP is a major mediator of pancreatic β-cell dysfunction, one of the most important genes regulated in response to hyperglycemia. It inhibits glucose uptake and promotes the cleavage of caspase-1, which leads to glucose-dependent β-cell death [ 23 ]. Fructose-incubated U and THP-1 cells have been shown to increase ROS production and expression of IL-1β, IL, and caspase-1 genes and proteins, all of which are evidence of NLRP3 inflammasome activity in these cells.

Interestingly, the treatment of human and mouse macrophages with fructose increases the rate of NLRP3 exposure to TXNIP in the cytosol and thus activates NLRP3 inflammasome. The results of this study showed that quercetin and ascorbic acid owing to their antioxidant properties can prevent the activation of NLRP3 inflammasome through TXNIP and thus prevent the exacerbation of inflammation [ 24 ].

Other studies have also reported that the quercetin prevents the NLRP3 inflammasome activation through TXNIP. For example, a study evaluated the molecular mechanism of quercetin in rat models of spinal cord injury SCI.

The results revealed a significant increase in NLRP3 inflammasome activity, a sharp increase in proinflammatory cytokine production and secretion, and a significant reduction in the rate of ROS production by the quercetin in the SCI rats.

An increase in ROS concentration has been identified as one of the prominent NLRP3 inflammasome stimulants that occur through TXNIP. Previous studies have shown that the quercetin is also a TXNIP inhibitor.

In addition, the quercetin, as expected, was also able to inhibit the proinflammatory cytokine production and the NLRP3 inflammasome activation in these rats.

In addition, the quercetin improved histopathological conditions and motor status in the SCI rats. This study also confirmed the anti-inflammatory effects of quercetin besides its therapeutic potential in diseases with inflammatory background and NLRP3 inflammasome activity, which is a known factor in the immunopathogenesis of COVID [ 25 ].

In a study, differentiated THP-1 cells were treated with the monosodium urate MSU crystals to activate NLRP3 inflammasome. Of the 56 flavonoids tested, only flavone, apigenin, kaempferol and quercetin were significantly reduced the IL-1β production [ 26 ].

Diabetic nephropathy DN is one of the most debilitating consequences for people with diabetes. Overactivation of NLRP3 inflammasome due to overproduction of ROS and high glucose levels is one of the important factors in DN immunopathogenesis. A study of DN rats found that Dihydroquercetin DHQ besides other effects was able to effectively prevent the overproduction of ROS in the rat kidney cells and ultimately the activation of NLRP3 inflammasome.

By inhibiting destructive inflammation, the DHQ thus prevented severe renal cell damage and eventually the risk of DN. This study showed well how quercetin is able to act as an effective anti-inflammatory factor by inhibiting NLRP3 inflammasome [ 27 ].

In a study, researchers investigated the possible role of TXNIP in type 1 diabetes-associated non-alcoholic fatty liver disease NFALD in the rat BRL-3A and human HepG2 cells. The results showed that the activation of NLRP3 inflammasome due to increased ROS production and under the influence of TXNIP factor plays a major role in the incidence of the disease.

Severe inflammation plays a key role in the immunopathogenesis of these diseases. Quercetin and allopurinol significantly increased TXNIP expression, as well as inhibited NLRP3 inflammasome activation, increased SREBP-1c and SREBP-2, and synthesized fatty acids, increased ROS and IL-1β secretion in diabetic rat liver.

Finally, the findings of this study showed that targeting liver TXNIP by quercetin and allopurinol may be a therapeutic target in the prevention of type 1 diabetes-associated NAFLD [ 28 ]. This signaling pathway eventually exacerbates inflammation, increases IL-1β production and kills endothelial cells.

Quercetin, Luteolin and Epigallocatechin gallate EGCG reduce ROS production and inhibit TXNIP-NLRP3 inflammasome in endothelial cells and reduce their IL-1β production. In addition, these agents protect endothelial cells from death by apoptosis through the restoration of mitochondrial membrane potential Deltapsim and the inhibition of caspase-3 activity [ 29 ].

The results of this study clearly show how quercetin, while acting as an antioxidant and anti-inflammatory factor, can prevent the cells from apoptosis by inhibiting the apoptotic process. Evidence from patients with the severe form of COVID shows high cellular degeneration besides severe inflammation, and these results clearly illustrate why quercetin can be a potential treatment for COVID A study evaluated the effect of quercetin on the hypothalamus of high-fructose-fed rats.

Through this mechanism, the quercetin can reduce the hypothalamic inflammatory lesions [ 30 ]. Interestingly, the quercetin was able to increase the expression of SIRT1 and decrease the expression of NLRP3 inflammasome components such as NLRP3 and adapter protein ASC and activated caspase The quercetin also decreased the expression of proinflammatory cytokines, such as IL-1β and IL [ 31 ].

The findings of this study are extremely important because SIRT1 is a pivotal factor. The SIRT1 is a class III histone deacetylases, involved in regulating various physiological processes, including cellular inflammation and metabolism.

Emerging evidence has shown that the SIRT1 not only downregulates the NF-κB signaling pathway but also has anti-inflammatory functions in several tissues.

The level of SIRT1 expression decreases with age. Studies have shown that the SIRT1 activation may be at least partially responsible for increasing life expectancy in mammals.

Aging in humans is associated with chronic and mild inflammation called Inflammaging, predisposing many age-related chronic diseases [ 32 ]. The NF-κB is the main regulator in the development of the Inflammaging. A recent study reported that the SIRT1 is a potential therapeutic target for the prevention of pregnancy-related complications associated with inflammation [ 34 ].

Another study shows that the SIRT1 suppresses acute pulmonary inflammation during sepsis by controlling the NLRP3 inflammasome activation [ 35 ]. The NLRP3 inflammasome is involved in various central nervous system disorders by exacerbating the inflammation.

In this study, it was found that the SIRT1 improved these disorders by inhibiting the NLRP3 inflammasome [ 36 ]. Another study found that the Doxofylline inhibited NLRP3 inflammasome via SIRT1 and thus prevented inflammation in lung epithelial cells [ 37 ]. Studies have shown that the GD15 is able to prevent acute pulmonary inflammation by increasing the expression of SIRT1 in the inflammation-caused lung injury of rats following the NLRP3 inflammasome activation [ 38 ].

The NLRP3 inflammasome is involved in the development of various Central nervous system CNS disorders by exacerbating the inflammation.

The SIRT1 was able to help improve these disorders through the NLRP3 inflammasome inhibition [ 36 ]. Gut microbiota has a profound effect on the homeostasis of local and systemic immune responses [ 39 ]. The association of dysbiosis with a range of diseases has been recognized, and inflammatory diseases are also affected by gut microbiome [ 40 ].

A study evaluated the effect of quercetin on gut microbiome balance and related gut-liver axis activation in rat models of NFALD and obesity. Metagenomic studies have shown the gut microbiome imbalance, called dysbiosis.

pylori bacteria. Dysbiosis further exacerbates inflammation in a variety of ways. However, the quercetin restores the gut microbiome imbalance and leads to the cessation of the dysregulation of the expression of genes related to lipid metabolism by inhibiting the NLRP3 inflammasome activation caused by endotoxinemia [ 41 ].

This study is important because basically the inflammation caused by metabolism and the wrong lifestyle called metainflammation is a suitable platform for many inflammatory diseases, and it seems that the deadly reaction of the immune system of a group of people with COVID is due to this type of inflammatory underlying causes.

Bacterial infections, such as E. The findings showed that the quercetin could prevent NLRP3 inflammasome activation in E. coli O H7 infection by maintaining the mitochondrial membrane integrity and inhibiting mitochondrial ROS release to cytosol. The E. coli O H7 infection inhibits autophagy in the host cell.

However, the quercetin by increasing the autophagy prevents overproduction of ROS and production of IL-1β and IL [ 42 ]. Increased quercetin-mediated autophagy to prevent further inflammation is one of the most important findings of this study, which could be another reason for the positive effect of quercetin in the treatment of COVID A study investigated the effect of extracts of water dropwort EWD and pharmacological molecules derived from hyperoside and isorhamnetin, which are derivatives of quercetin, on inflammatory responses especially NLRP3 inflammasome activation.

The anti-NLRP3 inflammasome function of EWD, hyperoside and isorhamnetin has been well demonstrated in human and mouse macrophages. The EWD reduced the IL-1β secretion. In addition, it inhibited the formation of pyroptosome from NLRC4, NLRP3, and AIM2 inflammasomes without disturbing the expression of cytokines.

The isorhamnetin selectively inhibited the activation of AIM2 and NLRP3 inflammasomes and the secretion of proinflammatory cytokine. The hyperoside selectively impaired the activation of AIM2 and NLRC4 inflammasomes, but not proinflammatory cytokine expression. In addition, all three EWD, isorhamnetin and hyperoside effectively inhibited caspase-1 activity.

Therefore, hyperoside and isorhamnetin, as compounds derived from quercetin, can be considered as anti-inflammatory compounds, especially as NLRP3 inflammasome inhibitors [ 43 ]. A study evaluated the effect of three flavonoids of quercetin, naringenin and silymarin on the NLRP3 inflammasome activation.

The results showed that quercetin was able to inhibit the activation of NLRP3 and AIM2 inflammasomes, but not NLRC4 inflammasome. The results of this study also showed that the effects of the above compounds occur in a completely independent way of autophagy. In addition, the quercetin inhibits the ASC oligomerization, which is essential for the NLRP3 inflammasome activation.

Recent studies have shown the destructive role of TH17 lymphocytes and neutrophils as type 3 inflammation in many autoimmune disorders and inflammatory diseases. In fact, the imbalance between TH17 and its produced cytokines with Treg and its cytokines is a key phenomenon in the immunopathogenesis of many severe inflammatory diseases.

Studies in animal models as well as patients with COVID have shown severe neutrophil infiltration into lung tissue. In addition, various studies reported an increase in serum IL in patients. Interestingly, the quercetin reduced THrelated cytokines such as ILA and IL and increased Treg-related cytokines such as IL and TGF-β.

Moreover, the quercetin reduced the percentage of Th17 cells and increased the percentage of Treg cells. In addition, a decrease in the NLRP3 inflammasome activation, IL-1β and caspase-1 was also clearly observed as a result of quercetin treatment.

The quercetin also reduced inflammatory mediators including TNF-α, IL-1β, IL-6, PGE2, COX-2 and iNOS significantly. Importantly, all of the therapeutic effects mentioned for quercetin were lost as a result of the anti-HO1 siRNA. In another study, the fructose was used to induce hyperuricemia and dyslipidemia in rats, which activated NLRP3 inflammasome in kidney cells.

Subsequently, the fructose-induced hyperuricemia and dyslipidemia were treated by allopurinol, quercetin and NLRP3 inflammasome inhibitors to improve signaling disturbances and reduce lipid accumulation. The results showed that a combination of the uric acid-lowering drug, allopurinol, and quercetin, as the NLRP3 inflammasome inhibitor, could play a key role in the immunopathogenesis in patients with severe inflammation caused by NLRP3 inflammasome activity [ 45 ].

In a study, IFN-γ-primed keratinocytes were treated with double-stranded DNA viruses, called poly dA: dT. In fact, this activates the AIM2 inflammasome. These cells were subsequently incubated by quercetin.

The inhibitory effect is due to the reduction of AIM2 and pro-caspase1 expression by the quercetin. This study actually shows another aspect of quercetin inhibitory potential in situations where severe inflammation is caused by viral invasion [ 46 ].

Many studies have shown that the quercetin acts as a protective factor in chronic cardiovascular disease CVD and related risk factors. Atherosclerosis is the leading cause of CVD that is reduced by using oral quercetin in animal models. The macrophages are one of the main innate immune cells involved in the development of atherosclerosis.

The results of this study showed that the quercetin, like other similar substances, inhibited the ROS production and IL-6 secretion in oxLDL-stimulated macrophages. The quercetin also inhibited the production of IL-1β followed by NLRP3 inflammasome activation under the influence of cholesterol crystals.

apolipoprotein E-knockout mouse models of dyslipidemia intraperitoneally treated with quercetin showed smaller atheromatous lesions, decreased atherosclerosis, decreased of inflammatory lymphocyte and macrophage infiltration through coronary arteries [ 47 ]. It should be noted that severe inflammation, extensive infiltration of monocytes, lymphocytes and neutrophils, and overproduction of proinflammatory cytokine all play a key role in COVID immunopathogenesis, especially in severe cases of acute lung injury ALI and acute respiratory distress syndrome ARDS ; accordingly, this study also shows the possible therapeutic effect of quercetin in COVID A study evaluated the anti-inflammatory and analgesic effects of quercetin in MSU-induced gout.

The study also compared the sensitivity of quercetin effects with naloxone, as a mu-opioid receptor antagonist. The results demonstrated that the quercetin inhibited MSU-induced mechanical hyperalgesia, leukocyte recruitment, production of TNFα and IL-1β, production of superoxide anion, NLRP3 inflammasome activation, NF-κB activation and expression of NLRP3 inflammasome complex mRNA.

The pre-treatment of naloxone prevented all inhibitory effects of quercetin on MSU-induced gout. These results showed that the quercetin exerts its analgesic and anti-inflammatory effects on MSU-induced gout in a naloxone-sensitive manner [ 48 ].

Alcoholic hepatitis is characterized by inflammation and necrosis of the liver tissue due to excessive intake of alcohol and sometimes even causes liver failure. Oxidative stress and NLRP3 inflammasome activation play a key role in the immunopathogenesis of this destructive disease.

The quercetin can increase Nrf2 expression and improve acute alcohol-induced liver injury in rats. Meanwhile, the quercetin also increases the anti-inflammatory factor IL independent of HO1. Thus, the quercetin increases IL and HO-1 expression by inhibiting NLRP3 inflammasome activation and inflammatory factor secretion, and maintaining liver function in acute alcohol-induced injury [ 49 ].

The findings of this study raise hopes for a positive effect of quercetin to control the life-threatening uncontrolled inflammation in the patients with COVID [ 49 ]. A clinical trial on the effect of Quercetin on the prevention and treatment of COVID has been registered in ClinicalTrials.

gov with the ID code NCT The results of this trial have not been published as of this writing. In Iran, we are conducting a clinical trial with the ID code IRCTN2 to determine the effect of Quercetin on the efficacy of antiviral drug regimen in COVID patients.

In a recent study [ 43 ], researchers have assessed the ability of secondary metabolites extracted from Aframomum melegueta to inhibit host furin. It has been shown that, like EBOLA and HIV, SARS-CoV-2 has a unique furin-like cleavage site FCS , RRAR , which makes it several times more contagious than other beta-coronaviruses such as SARS-CoV [ 50 ].

Findings have shown that flavonoids such as Apigenin, Tectochrysin, and Quercetin have high binding power to SARS-CoV-2 targets. In a bioinformatics study, researchers have investigated the potential of compounds derived from Moringaoleifera in inhibiting SARS-CoV-2 proteases and made a comparison with known antiviral drugs.

The results of this study have clearly demonstrated that much similar to well-known antiviral drugs like Lopinavir-Ritonavir, Maraviroc, Nelnavir, and Tipranavir, flavonoid compounds such as isoquercetin, quercetin, and dihydroquercetin can potentially exhibit antiviral properties through the inhibition of SARS-CoV-2 proteases like Mpro.

In addition to this potential antiviral property, these compounds also have antioxidant properties that can help limit the damage of the severe form of COVID [ 51 ]. The SARS-CoV-2 pandemic has caused the death of over 1,, people. Acute respiratory distress syndrome and acute lung injury resulting from cytokine storm and severe inflammation are considered as the leading cause of death in patients with severe COVID Many clinical trials are currently underway to alleviate this destructive inflammation.

The NLRP3 inflammasome inhibition, owing to its key role in inflammation, can be a more efficient, cost-effective and accurate method than merely inhibiting cytokines.

The quercetin has an interesting inhibitory effect on inflammatory responses. On the other hand, it not only inhibits the production of NLRP3 inflammasome components and pro-IL-1β, but also suppresses inflammation through interference in various signaling pathways, especially NF-κB.

The NLRP3 inflammasome is affected by regulators such as TXNIP, SIRT1 and NRF2, which play a key role in the activation or inhibition of the NLRP3 inflammasome.

The quercetin also has an effect on these factors, thereby suppressing NLRP3 inflammasome and eventually inflammation. TH17 and its associated cytokines play an important role in inflammatory diseases through neutrophil recruitment.

The neutrophil recruitment and activation in COVID have also been well demonstrated. The inhibitory effects of quercetin on IL can double the hope for a positive outcome in the treatment of COVID Gut microbiota has an unparalleled function in the regulation of immune responses and the development of a variety of diseases caused by aberrant immune responses.

The effect of quercetin on the correct dysbiosis can help control systemic inflammation in the body. Finally, the quercetin, as an anti-inflammatory, antioxidant, analgesic and NLRP3 inflammasome inhibitor compound, can be a potential treatment for severe inflammation, which is the main life-threatening condition in patients with COVID Wu F, Zhao S, Yu B, Chen Y-M, Wang W, Song Z-G, Hu Y, Tao Z-W, Tian J-H, Pei Y-Y.

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J Med Virol. Mao L, Wang M, Chen S, He Q, Chang J, Hong C, Zhou Y, Wang D, Miao X, Hu Y: Neurological manifestations of hospitalized patients with COVID in Wuhan, China: a retrospective case series study.

Zhou P, Yang X-L, Wang X-G, Hu B, Zhang L, Zhang W, Si H-R, Zhu Y, Li B, Huang C-L. A pneumonia outbreak associated with a new coronavirus of probable bat origin.

Huang C, Wang Y, Li X, Ren L, Zhao J, Hu Y, Zhang L, Fan G, Xu J, Gu X. Clinical features of patients infected with novel coronavirus in Wuhan, China.

Chen N, Zhou M, Dong X, Qu J, Gong F, Han Y, Qiu Y, Wang J, Liu Y, Wei Y. Epidemiological and clinical characteristics of 99 cases of novel coronavirus pneumonia in Wuhan, China: a descriptive study.

Wang D, Hu B, Hu C, Zhu F, Liu X, Zhang J, Wang B, Xiang H, Cheng Z, Xiong Y. Clinical characteristics of hospitalized patients with novel coronavirus—infected pneumonia in Wuhan, China. Zahid A, Li B, Kombe JK, Jin T, Tao J.

Pharmacological inhibitors of the NLRP3 NLRP3 inflammasome. Front Immunol. Article PubMed PubMed Central CAS Google Scholar. Zhao C, Zhao W. NLRP3 NLRP3 inflammasome —a key player in antiviral responses. Panche A, Diwan A, Chandra S. Flavonoids: an overview. J Nutr Sci. Kelly GS.

Altern Med Rev. PubMed Google Scholar. Hollman PC, de Vries JH, van Leeuwen SD, Mengelers MJ, Katan MB. Absorption of dietary quercetin glycosides and quercetin in healthy ileostomy volunteers.

Am J Clin Nutr. Article CAS PubMed Google Scholar. Swanson KV, Deng M, Ting JP-Y. The NLRP3 NLRP3 inflammasome : molecular activation and regulation to therapeutics. Nat Rev Immunol.

Dinarello CA, Simon A, Van Der Meer JW. Treating inflammation by blocking interleukin-1 in a broad spectrum of diseases. Nat Rev Drug Discov.

Walle LV, Stowe IB, Šácha P, Lee BL, Demon D, Fossoul A, Van Hauwermeiren F, Saavedra PH, Šimon P, Šubrt V. PLoS Biol. Article CAS Google Scholar. Coll RC, Robertson AA, Chae JJ, Higgins SC, Muñoz-Planillo R, Inserra MC, Vetter I, Dungan LS, Monks BG, Stutz A. A small-molecule inhibitor of the NLRP3 NLRP3 inflammasome for the treatment of inflammatory diseases.

Nat Med. Dempsey C, Araiz AR, Bryson K, Finucane O, Larkin C, Mills E, Robertson A, Cooper M, O'Neill L, Lynch M.

Brain Behav Immun. van der Heijden T, Kritikou E, Venema W, van Duijn J, van Santbrink PJ, Slütter B, Foks AC, Bot I, Kuiper J. NLRP3 NLRP3 inflammasome inhibition by MCC reduces atherosclerotic lesion development in apolipoprotein E—deficient mice—brief report.

Arterioscler Thromb Vasc Biol. Article PubMed CAS Google Scholar. Monnerat G, Alarcón ML, Vasconcellos LR, Hochman-Mendez C, Brasil G, Bassani RA, Casis O, Malan D, Travassos LH, Sepúlveda M. Macrophage-dependent IL-1β production induces cardiac arrhythmias in diabetic mice.

Nat Commun. Mangan MS, Olhava EJ, Roush WR, Seidel HM, Glick GD, Latz E. Targeting the NLRP3 NLRP3 inflammasome in inflammatory diseases. Mahmood DF, Abderrazak A, El Hadri K, Simmet T, Rouis M. The thioredoxin system as a therapeutic target in human health and disease.

Antioxid Redox Signal. Zhou R, Tardivel A, Thorens B, Choi I, Tschopp J. Thioredoxin-interacting protein links oxidative stress to NLRP3 inflammasome activation. Nat Immunol. Guo H, Callaway JB, Ting JP. NLRP3 inflammasome s: mechanism of action, role in disease, and therapeutics. Choe J-Y, Kim S-K.

Quercetin and ascorbic acid suppress fructose-induced NLRP3 NLRP3 inflammasome activation by blocking intracellular shuttling of TXNIP in human macrophage cell lines. Jiang W, Huang Y, Han N, He F, Li M, Bian Z, Liu J, Sun T, Zhu L. Quercetin suppresses NLRP3 NLRP3 inflammasome activation and attenuates histopathology in a rat model of spinal cord injury.

Spinal Cord. Lim H, Min DS, Park H, Kim HP. Flavonoids interfere with NLRP3 NLRP3 inflammasome activation.

The NLRP3 inflammasome is affected by regulators such as TXNIP, SIRT1 and NRF2, which play a key role in the activation or inhibition of the NLRP3 inflammasome. The quercetin also has an effect on these factors, thereby suppressing NLRP3 inflammasome and eventually inflammation.

TH17 and its associated cytokines play an important role in inflammatory diseases through neutrophil recruitment. The neutrophil recruitment and activation in COVID have also been well demonstrated. The inhibitory effects of quercetin on IL can double the hope for a positive outcome in the treatment of COVID Gut microbiota has an unparalleled function in the regulation of immune responses and the development of a variety of diseases caused by aberrant immune responses.

The effect of quercetin on the correct dysbiosis can help control systemic inflammation in the body. Finally, the quercetin, as an anti-inflammatory, antioxidant, analgesic and NLRP3 inflammasome inhibitor compound, can be a potential treatment for severe inflammation, which is the main life-threatening condition in patients with COVID Wu F, Zhao S, Yu B, Chen Y-M, Wang W, Song Z-G, Hu Y, Tao Z-W, Tian J-H, Pei Y-Y.

A new coronavirus associated with human respiratory disease in China. Article CAS PubMed PubMed Central Google Scholar. Li YC, Bai WZ, Hashikawa T. The neuroinvasive potential of SARS-CoV2 may play a role in the respiratory failure of COVID patients. J Med Virol. Mao L, Wang M, Chen S, He Q, Chang J, Hong C, Zhou Y, Wang D, Miao X, Hu Y: Neurological manifestations of hospitalized patients with COVID in Wuhan, China: a retrospective case series study.

Zhou P, Yang X-L, Wang X-G, Hu B, Zhang L, Zhang W, Si H-R, Zhu Y, Li B, Huang C-L. A pneumonia outbreak associated with a new coronavirus of probable bat origin.

Huang C, Wang Y, Li X, Ren L, Zhao J, Hu Y, Zhang L, Fan G, Xu J, Gu X. Clinical features of patients infected with novel coronavirus in Wuhan, China.

Chen N, Zhou M, Dong X, Qu J, Gong F, Han Y, Qiu Y, Wang J, Liu Y, Wei Y. Epidemiological and clinical characteristics of 99 cases of novel coronavirus pneumonia in Wuhan, China: a descriptive study.

Wang D, Hu B, Hu C, Zhu F, Liu X, Zhang J, Wang B, Xiang H, Cheng Z, Xiong Y. Clinical characteristics of hospitalized patients with novel coronavirus—infected pneumonia in Wuhan, China.

Zahid A, Li B, Kombe JK, Jin T, Tao J. Pharmacological inhibitors of the NLRP3 NLRP3 inflammasome. Front Immunol. Article PubMed PubMed Central CAS Google Scholar. Zhao C, Zhao W. NLRP3 NLRP3 inflammasome —a key player in antiviral responses.

Panche A, Diwan A, Chandra S. Flavonoids: an overview. J Nutr Sci. Kelly GS. Altern Med Rev. PubMed Google Scholar. Hollman PC, de Vries JH, van Leeuwen SD, Mengelers MJ, Katan MB.

Absorption of dietary quercetin glycosides and quercetin in healthy ileostomy volunteers. Am J Clin Nutr. Article CAS PubMed Google Scholar. Swanson KV, Deng M, Ting JP-Y. The NLRP3 NLRP3 inflammasome : molecular activation and regulation to therapeutics. Nat Rev Immunol.

Dinarello CA, Simon A, Van Der Meer JW. Treating inflammation by blocking interleukin-1 in a broad spectrum of diseases. Nat Rev Drug Discov. Walle LV, Stowe IB, Šácha P, Lee BL, Demon D, Fossoul A, Van Hauwermeiren F, Saavedra PH, Šimon P, Šubrt V.

PLoS Biol. Article CAS Google Scholar. Coll RC, Robertson AA, Chae JJ, Higgins SC, Muñoz-Planillo R, Inserra MC, Vetter I, Dungan LS, Monks BG, Stutz A. A small-molecule inhibitor of the NLRP3 NLRP3 inflammasome for the treatment of inflammatory diseases.

Nat Med. Dempsey C, Araiz AR, Bryson K, Finucane O, Larkin C, Mills E, Robertson A, Cooper M, O'Neill L, Lynch M.

Brain Behav Immun. van der Heijden T, Kritikou E, Venema W, van Duijn J, van Santbrink PJ, Slütter B, Foks AC, Bot I, Kuiper J. NLRP3 NLRP3 inflammasome inhibition by MCC reduces atherosclerotic lesion development in apolipoprotein E—deficient mice—brief report.

Arterioscler Thromb Vasc Biol. Article PubMed CAS Google Scholar. Monnerat G, Alarcón ML, Vasconcellos LR, Hochman-Mendez C, Brasil G, Bassani RA, Casis O, Malan D, Travassos LH, Sepúlveda M. Macrophage-dependent IL-1β production induces cardiac arrhythmias in diabetic mice.

Nat Commun. Mangan MS, Olhava EJ, Roush WR, Seidel HM, Glick GD, Latz E. Targeting the NLRP3 NLRP3 inflammasome in inflammatory diseases. Mahmood DF, Abderrazak A, El Hadri K, Simmet T, Rouis M. The thioredoxin system as a therapeutic target in human health and disease.

Antioxid Redox Signal. Zhou R, Tardivel A, Thorens B, Choi I, Tschopp J. Thioredoxin-interacting protein links oxidative stress to NLRP3 inflammasome activation.

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Jiang W, Huang Y, Han N, He F, Li M, Bian Z, Liu J, Sun T, Zhu L. Quercetin suppresses NLRP3 NLRP3 inflammasome activation and attenuates histopathology in a rat model of spinal cord injury. Spinal Cord. Lim H, Min DS, Park H, Kim HP. Flavonoids interfere with NLRP3 NLRP3 inflammasome activation.

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Download references. The authors wish to acknowledge the support prepared by Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran. Department of Immunology, Faculty of Medicine, Ahvaz Jundishapur University of Medical, Sciences, Ahvaz, Iran. ImmunologyToday, Universal Scientific Education and Research Network USERN , Tehran, Iran.

Thalassemia and Hemoglobinopathy Research Center, Health Research Institute, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran. You can also search for this author in PubMed Google Scholar. Ali Saeedi-Boroujeni and Mohammad-Reza Mahmoudian-Sani designed the study and data collection and analysis.

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Saeedi-Boroujeni, A. Anti-inflammatory potential of Quercetin in COVID treatment. J Inflamm 18 , 3 Download citation. Received : 16 June Accepted : 21 January Published : 28 January Anyone you share the following link with will be able to read this content:.

Sorry, a shareable link is not currently available for this article. Provided by the Springer Nature SharedIt content-sharing initiative. Skip to main content. Search all BMC articles Search. Download PDF. Abstract SARS-CoV-2 is a betacoronavirus causing severe inflammatory pneumonia, so that excessive inflammation is considered a risk factor for the disease.

Introduction Acute respiratory infection was reported in several patients in Wuhan, Hubei Province, China in December A body of literature NLRP3 inflammasome Pattern Recognition Receptors PRRs are among the key components of the innate immune system.

Flavonoids and quercetin as anti-inflammatory and NLRP3 inflammasome inhibitors Flavonoids, or phenolic acids, belong to the group of water-soluble plant pigments, which are responsible for the antioxidant capacity of fruits and plants. Importance of NLRP3 inflammasome inhibition in the treatment of inflammatory diseases The NLRP3 inflammasome is one of the most important research areas in immunology.

Quercetin inhibits NLRP3 inflammasome by affecting TXNIP Fructose-incubated U and THP-1 cells have been shown to increase ROS production and expression of IL-1β, IL, and caspase-1 genes and proteins, all of which are evidence of NLRP3 inflammasome activity in these cells.

Effect of quercetin on gut microbiome Gut microbiota has a profound effect on the homeostasis of local and systemic immune responses [ 39 ]. Quercetin and autophagy Bacterial infections, such as E. Quercetin in metabolic syndrome In another study, the fructose was used to induce hyperuricemia and dyslipidemia in rats, which activated NLRP3 inflammasome in kidney cells.

Effect of quercetin on the AIM2 inflammasome pathway In a study, IFN-γ-primed keratinocytes were treated with double-stranded DNA viruses, called poly dA: dT.

Effect of quercetin on inflammatory macrophages Many studies have shown that the quercetin acts as a protective factor in chronic cardiovascular disease CVD and related risk factors. Quercetin as an analgesic and anti-inflammatory A study evaluated the anti-inflammatory and analgesic effects of quercetin in MSU-induced gout.

Molecular mechanisms of Quercetin action to manage COVID Full size image. Conclusion The SARS-CoV-2 pandemic has caused the death of over 1,, people.

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Article CAS PubMed Google Scholar Lanzillotta A, Sarnico I, Ingrassia R, Boroni F, Branca C, Benarese M, Faraco G, Blasi F, Chiarugi A, Spano P. If you are taking any medication, talk with your healthcare provider about any potential risk there is before starting quercetin.

As with any supplement, quercetin isn't regulated by the FDA. To ensure what you are buying was manufactured correctly, is true to the ingredient list, and doesn't contain harmful levels of contaminants, purchase a product that has been third-party tested.

Reputable third-party testing organizations include ConsumerLab, NSF International, and U. Kidney damage has been reported but only with the use of intravenous quercetin in large amounts.

It's unknown how safe large doses or long-term use of oral quercetin supplementation is. Generally, quercetin is considered to be safe when gotten naturally through food and drinks.

While less is known about quercetin supplements, no serious side effects have been reported in clinical trials that used up to 1, mg a day for up to 12 weeks. One study that used mg of quercetin twice daily for 30 days did show mild effects. These effects included stomach pain and reflux, constipation , diarrhea , gas , and sleep disorders.

However, the rate of these effects was similar to that of the placebo group. Quercetin, a plant pigment specifically known as a flavonoid, has antioxidant and anti-inflammatory effects.

It is readily available in a variety of whole, plant-based foods and tea. You can also take quercetin in supplement form. While quercetin supplements have been studied for certain medical conditions, there are currently no guidelines or recommendations for the use of these supplements for general health or disease prevention.

If you are interested in taking quercetin, speak with your healthcare provider first to hear more about its potential benefits and side effects based on your specific health. Lee JS, Cha TJ, Lee KH, Yim JE. Onion peel extract reduces the percentage of body fat in overweight and obese subjects: A week, randomized, double-blind, placebo-controlled study.

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ACS Omega. Li Y, Yao J, Han C, et al. Quercetin, inflammation and immunity. National Institutes of Health Office of Dietary Supplements. Dietary supplements in the time of COVID Botanical dietary supplements background information. Use limited data to select advertising.

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