Nature Wins Quercetin Plus (30 Count)

The Effect of Quercetin on Inflammatory Factors and Clinical Symptoms in Women with Rheumatoid Arthritis: A Double-Blind, Randomized Controlled Trial

• https://www.tandfonline.com/doi/full/10.1080/07315724.2016.1140093
• The present study was a randomized, double-blind, placebo-controlled clinical trial in which 50 women with RA were allocated into a quercetin (500 mg/day) or placebo group for 8 weeks.
• Quercetin supplementation for 8 weeks significantly reduced EMS, morning pain, and after-activity pain (p < 0.05). DAS-28 and HAQ scores decreased in the quercetin group compared to placebo and the number of patients with active disease significantly decreased in the quercetin group.
• Plasma hs-TNFα level was significantly reduced in the quercetin group compared to placebo (p < 0.05).
• TJC significantly decreased in the quercetin group after the intervention. Supplementation had an effect on ESR but it was not significant (p > 0.05).
• Five hundred milligrams per day quercetin supplementation for 8 weeks resulted in significant improvements in clinical symptoms, disease activity, hs-TNFα, and HAQ in women with RA.

In vitro and in vivo evidence that quercetin protects against diabetes and its complications: A systematic review of the literature

• https://www.sciencedirect.com/science/article/pii/S0753332218349187?via%3Dihub
• The commonly used doses and treatment cycles of QE derived from the literature have been presented as follows: 30 mg/kg body weight (bw) for 14 days [38]; 10 and 15 mg/kg. bw for 2 weeks[39] and 8 weeks [37]; 50 and 80 mg/kg bw for 45 days [40]; 100 mg/kg.bw for 49 days [41]; 25, 50 and 75 mg/kg for 28 days [42]; 100 and 200 mg/kg bw for 6 weeks [43]. Moreover, dietary QE (0.5% in the diet) was also effective in ameliorating the increased levels of fasting blood glucose, urine sugar, and urine volume in STZ induced diabetic rats
• oral administration of QE (15–100) for 14–70 days resulted in a significant reduction in blood glucose by regenerating pancreatic islets, increasing of serum insulin level and promoting insulin release in diabetes rat models. In high fat diet (HFD) induced insulin resistance [44]and type 2 diabetes C57BL/KsJ-db/db mice models
• QE could significantly increase plasma insulin levels and reduce blood glucose by maintaining β-cells mass and function
• QE is suitable for prevention and treatment of diabetic nephropathy due to its hypoglycemic property, antioxidant activity, and anti-inflammatory capacity [10]. QE can also decrease the fasting blood glucose level in streptozotocin (STZ)-induced type 1 diabetic rats

Effects of Quercetin on Blood Pressure: A Systematic Review and Meta-Analysis of Randomized Controlled Trials

• https://www.ahajournals.org/doi/10.1161/JAHA.115.002713
• Effect size was expressed as weighted mean difference (WMD) and 95% CI. Overall, the impact of quercetin on BP was reported in 7 trials comprising 9 treatment arms (587 patients)
• The results of the meta-analysis showed significant reductions both in systolic BP (WMD: -3.04 mm Hg, 95% CI: -5.75, -0.33, P=0.028) and diastolic BP (WMD: -2.63 mm Hg, 95% CI: -3.26, -2.01, P<0.001) following supplementation with quercetin. When the studies were categorized according to the quercetin dose, there was a significant systolic BP and diastolic BP-reducing effect in randomized controlled trials with doses ≥500 mg/day (WMD: -4.45 mm Hg, 95% CI: -7.70, -1.21, P=0.007 and -2.98 mm Hg, 95% CI: -3.64, -2.31, P<0.001, respectively), and lack of a significant effect for doses <500 mg/day (WMD: -1.59 mm Hg, 95% CI: -4.44, 1.25, P=0.273 and -0.24 mm Hg, 95% CI: -2.00, 1.52, P=0.788, respectively), but indirect comparison tests failed to significant differences between doses.
• The results of the meta-analysis showed a statistically significant effect of quercetin supplementation in the reduction of BP, possibly limited to, or greater with dosages of >500 mg/day.

Quercetin enrich diet during the early-middle not middle-late stage of alzheimer’s disease ameliorates cognitive dysfunction

• https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5934583/
• Mice were divided into group mice received normal diet without any supplementation, and another group mice received diet supplemented with quercetin (2 mg/g diet).
• We first detected feeding mice a quercetin-enriched diet resulted in a significant improvement in the APP/PS1 mice
• quercetin enrich diet prevents AD pathological development through decreasing amyloid deposition and astrogliosis
• https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5934583/figure/fig01/
• The results showed that quercetin enrich diet (1 month-9 months) increased the time spent in target quadrant compared with normal diet
• quercetin enrich diet cover the early-middle stage of AD pathological development depress Aβ producing
• The results showed that quercetin enrich diet (1 month-9 months) significantly reduced the mRNA and protein level of Hevin and SPARC compared with normal diet.
• https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5934583/figure/fig02/
• The results showed that quercetin enrich diet (6 months-13 months) unaffected the mRNA and protein level of Hevin and SPARC compared with normal diet.
• https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5934583/figure/fig03/
• Research revealed that treatment of quercetin during the whole AD pathological development significantly prevented spatial cognitive dysfunction. Meanwhile, we found quercetin enrich diet only covered the early-middle stage (1 month-9 months) of AD pathology could reduce the Aβ accumulation by inhibiting of the amyloidogenic processing of APP according to the results from immunofluorescence and western blot
• Our data showed that quercetin enrich diet (1 month-13 month) significantly decreased the latency in APP/PS1 mice compared with the normal diet APP/PS1 mice

The flavonoid quercetin ameliorates Alzheimer's disease pathology and protects cognitive and emotional function in aged triple transgenic Alzheimer's disease model mice

• https://www.sciencedirect.com/science/article/abs/pii/S002839081500043X?via%3Dihub
• The worldwide prevalence of dementia is estimated to be as high as 36 million and is predicted to reach 66 million by 2030 and 115 million by 2050
• quercetin reliably exerts neuroprotective effects against agent-induced toxicity (Kanter et al., 2013) and increases the resistance of neurons to oxidative stress and excitotoxicity by modulating the mechanisms of cell death (Choi et al., 2014, Liu et al., 2013a)
• quercetin has been suggested to exert other beneficial effects on the central nervous system (CNS), such as anti-anxiety and cognitive enhancement, by stimulating or inhibiting enzyme activities/signal transduction pathways (Williams et al., 2004). However, whether quercetin reverses the primary histopathological hallmarks and the emotional and cognitive impairment of AD has yet to be determined.
• Quercetin treatment increased the cell density in the subiculum to a level similar to that in Non Tg mice treated with vehicle or quercetin (Fig. 2A, B)
• Our study is the first to provide a complete evaluation of the neuroprotective properties of quercetin as a therapeutic compound that ameliorates brain deficits in a triple transgenic AD mouse model. Quercetin treatment correlated to reversed brain levels of β-amyloidosis and tauopathy and ameliorated astroglial and microglial reactivity in the CA1 area, the subiculum, the EC and the amygdala

Restoring Effects of Natural Anti-Oxidant Quercetin on Cellular Senescent Human Dermal Fibroblasts

• https://www.worldscientific.com/doi/abs/10.1142/S0192415X18500453
• We examined the restoring properties of quercetin on human dermal fibroblasts (HDFs).
• Quercetin directly reduced either intracellular or extracellular ROS levels in aged HDFs. To find the aging-related target genes by quercetin, microarray analysis was performed and two up-regulated genes LPL and KCNE2 were identified.
• Silencing LPL increased the expression levels of senescence proteins such as p16INK4A and p53 and silencing KCNE2 reversed gene expressions of EGR1 and p-ERK in quercetin-treated aged HDFs. Silencing of LPL and KCNE2 decreased the expression levels of anti-oxidant enzymes such as superoxide dismutase and catalase.
• Also, the mitochondrial dysfunction in aged HDFs was ameliorated by quercetin treatment. Taken together, these results suggest that quercetin has restoring effect on the cellular senescence by down-regulation of senescence activities and up-regulation of the gene expressions of anti-oxidant enzymes in aged HDFs.

Quercetin in prostate cancer: Chemotherapeutic and chemopreventive effects, mechanisms and clinical application potential 

• https://www.spandidos-publications.com/or/33/6/2659
• Daily human intake of quercetin ranges from 10 to 100 mg depending on different dietary habits, and it can reach 500–1,000 mg if selected highly purified extracts are used
• Research has shown the anticancer property of quercetin in a variety of human cancer cell lines both in vitro and in vivo such as cervical, breast, colon (17) and lung carcinoma (18) and prostate cancer (19). Quercetin can effectively inhibit the growth of many types of tumors and is non-toxic
• When used in vitro, whether alone or in combination, quercetin greatly arrests the cell cycle, decreases cell viability, inhibits proliferation and induces cell apoptosis. Table I https://www.spandidos-publications.com/or/33/6/2659#tb_tI-or-33-06-2659 summarizes the in vitro effects of quercetin on prostate cancer. Similarly, when used in vivo, quercetin inhibits prostate cancer cell xenograft tumor growth effectively at the selective dose. Relevant results are summarized in Table II https://www.spandidos-publications.com/or/33/6/2659#tb_tII-or-33-06-2659
• Quercetin treatment not only resulted in an increase in the G2/M phase population in both PC-3 and LNCaP cells, but also increased the S phase population in PC-3 cells
• Liu et al treated human prostate cancer PC-3 cells with quercetin at various doses (50–200 μM) for 24 and 48 h and found that cell viability was significantly decreased in a time- and dose-dependent manner. It was attributed to induction of G0/G1 (31.4–49.7%) and sub-G1 (19.77%) cell cycle arrest which was caused by downregulation of cyclin D and E, CDK2, cdc25c and upregulation of p21, p53, p18 and p27
• In PPC1 prostate carcinoma cells, quercetin at a high dose arrested the cell cycle and inhibited proliferation
• Quercetin also displayed proliferation inhibition in a dose-dependent manner in PC-3 cells at a non-cytotoxic concentration, during which endoplasmic reticulum (ER)-mediated and ER-independent pathways as well as cell cycle inhibition induced by cyclin D1 and E downregulation may be the vital factors
• Quercetin, in addition to a decrease in anti-apoptotic Bcl-2 and an increase in pro-apoptotic Bax, ER stress-associated proteins such as GRP78, ATF-4α and IRE-1α were also increased, followed by direct activation of the caspase cascade leading to subsequent apoptosis through the mitochondrial pathway and ER stress
• Quercetin was found to enhance extrinsic apoptosis mediated by tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) in DU-145 cells either through DR5 upregulation or survivin downregulation via deacetylation of histone H-3 mediated by ERK in PC-3 and DU-145 cells or dephosphorylation of AKT in LNCaP and DU-145 cells
• it can be concluded that quercetin induces apoptosis of prostate cancer mainly by regulating Bax, Bcl-2 and the Bcl-2/Bax ratio, namely through mitochondrial-mediated intrinsic pathway, and it can also mediate the extrinsic pathway
• Treated LNCaP cells with quercetin and found that AR protein was reduced in a dose-dependent manner after a designated time. Moreover, the regulated tumor markers, PSA and hK2, were inhibited, and regulated genes such as PSA, NKX3.1 and ornithine decarboxylase (ODC) mRNA were downregulated. These findings indicate that quercetin not only decreases AR expression but also impairs the function of AR and has the potential to serve as a chemotherapeutic drug for prostate cancer

Health Benefits of Quercetin in Age-Related Diseases

• https://www.mdpi.com/1420-3049/27/8/2498
• Quercetin is among the widely occurring polyphenol, found abundantly in nature. It is commonly present in different plant products. Onion is known to have the highest quantity of quercetin. This plant compound is possessed antioxidant properties and is considered to have a protective function against aging.
• It is known to be present in both free and conjugated forms. Quercetin has anti-oxidative, anti-inflammatory, anti-proliferative, anti-carcinogenic, anti-diabetic, and anti-viral properties
• Various in vivo and in vitro studies have demonstrated the role of quercetin and here a detailed review of quercetin as a curative agent in neurodegeneration, diabetes, cancer, and inflammation has been carried out. Studies have proved that quercetin plays a crucial role in the prevention of age-related disorders.
• Quercetin is a potent antioxidant which is currently being used in various pharmaceuticals. Properties of quercetin can be further explored in various other disorders. Nanoformulations and liposomal formulations of quercetin can be made to treat other age associated diseases.
• https://www.mountsinai.org/health-library/supplement/quercetin#:~:text=Quercetin%20may%20help%20protect%20against,anti%2Dinflammatory%20and%20antihistamine%20effect
• Flavonoids, such as quercetin, are antioxidants. They scavenge particles in the body known as free radicals which damage cell membranes, tamper with DNA, and even cause cell death. Antioxidants can neutralize free radicals. They may reduce or even help prevent some of the damage free radicals cause. In test tubes, quercetin has strong antioxidant properties
• Quercetin may help protect against heart disease and cancer. Quercetin can also help stabilize the cells that release histamine in the body and thereby have an anti-inflammatory and antihistamine effect.