Anti-inflammatory Effects Of Quercetin Research Articles

Anti-Inflammatory Effects of Quercetin, Rutin, and Troxerutin Result From the Inhibition of NO Production and the Reduction of COX-2 Levels in RAW 264.7 Cells Treated with LPS.

Flavonols effectively scavenge the reactive nitrogen species (RNS) and reactive oxygen species (ROS) and act as immune-enhancing, anti-inflammatory, anti-diabetic, and anti-carcinogenic agents. Here, we explored the comparative antioxidant and anti-inflammatory properties of plant-originating flavonols, like quercetin, rutin, and troxerutin against acetylsalicylic acid. Quercetin and rutin showed a high ability to remove active ROS, but troxerutin and acetylsalicylic acid exhibited little such function. In RAW 264.7 cells, quercetin, rutin, and troxerutin did not exhibit cellular toxicity at low concentrations. In addition, quercetin, rutin, and troxerutin considerably (p < 0.05) lowered the protein expression of cyclooxygenase 2 (COX-2) as compared to acetylsalicylic acid in cells inflamed with lipopolysaccharides (LPS). Additionally, in inflamed cells, quercetin and rutin significantly down-regulated the nitrogen oxide (NO) level (p < 0.05) at higher concentrations, whereas Troxerutin did not reduce the NO level. In addition, Troxerutin down-regulated the pro-inflammatory protein markers, such as TNF-α, COX-2, NF-κB, and IL-1β better than quercetin, rutin, and acetylsalicylic acid. We observed that troxerutin exhibited a significantly greater anti-inflammatory effect than acetylsalicylic acid did. Acetylsalicylic acid did not significantly down-regulated the expression of COX-2 and TNF-α (p < 0.05) compared to troxerutin. Hence, it can be concluded that the down-regulation of NO levels and the expression of COX-2 and TNF-α proteins could be mechanisms of action for the natural compounds quercetin, rutin, and troxerutin in preventing inflammation.

Quercetin declines LPS induced inflammation and augments adiponectin expression in 3T3-L1 differentiated adipocytes SIRT-1 dependently.

Inflammation is an important factor contributing to obesity-induced metabolic disorders. Different investigations confirm that local inflammation in adipose issues is the primary reason for such disorder, resulting in low-grade systemic inflammation. Anti-inflammatory, antioxidant, and epigenetic modification are among the varied properties of Quercetin (QCT) as a natural flavonoid. The precise molecular mechanism followed by QCT to alleviate inflammation has been unclear. This study explores whether the anti-inflammatory effects of QCT in 3T3-L1 differentiated adipocytes may rely on SIRT-1. The authors isolated 3T3-L1 pre-adipocyte cells and exposed them to varying concentrations of QCT, lipopolysaccharide (LPS), and a selective inhibitor of silent mating type information regulation 2 homolog 1 (SIRT-1) called EX-527. After determining the optimal dosages of QCT, LPS, and EX-527, they assessed the mRNA expression levels of IL-18, IL-1, IL-6, TNF-α, SIRT-1, and adiponectin using quantitative reverse transcription-polymerase chain reaction (qRT-PCR). The study showed considerable cytotoxic effects of LPS (200 ng/mL) + QCT (100 µM) + EX-527 (10 µM) on 3T3-L1 differentiated adipocytes after 48h of incubation. QCT significantly upregulated the expression levels of adiponectin and SIRT-1 (p < 0.0001). However, introducing SIRT-1 inhibitor (p < 0.0001) reversed the impact of QCT on adiponectin expression. Additionally, QCT reduced SIRT-1-dependent pro-inflammatory cytokines in 3T3-L1 differentiated adipocytes (p < 0.0001). This study revealed that QCT treatment reduced crucial pro-inflammatory cytokines levels and increased adiponectin levels following LPS treatment. This finding implies that SIRT-1 may be a crucial factor for the anti-inflammatory activity of QCT.

Anti-inflammatory effect of quercetin in a murine model of lipopolysaccharide-induced acute lung injury: A systematic review

Acute lung injury (ALI) and its most severe form, acute respiratory distress syndrome (ARDS), are pulmonary manifestations of a systemic inflammation that causes thousands of deaths every year around the world. However, there are still no specific treatment for this disease. Thus, based on a systematic review, this study aimed to investigate the anti-inflammatory effects of quercetin in a murine lipopolysaccharide-induced acute lung injury model. The investigation was conducted in the PubMed, Science Direct, Web of Science, and Scopus databases via Periódicos Capes. Initially, 49 articles were found that went through screening and five studies were selected. The results showed that quercetin, when administered as a possible treatment for acute lung injury in mice, reduced markers of inflammation, such as MDA and NO levels, MPO activity, the accumulation of neutrophils in the lung, number of leukocytes in bronchoalveolar lavage (BAL), release of inflammatory cytokines TNF-α, IL-1β and IL-6 in BAL, pulmonary edema and infiltration in lung tissues.

Quercetin protects against Aspergillus fumigatus keratitis by reducing fungal load and inhibiting TLR-4 induced inflammatory response

PurposeTo investigate the antifungal and anti-inflammatory effects of quercetin in Aspergillus fumigatus (A. fumigatus) keratitis. MethodsDraize eye test was performed in mice to evaluate the toxicity of quercetin, and the antifungal effects on A. fumigatus were assessed via scanning electron microscopy (SEM), propidium iodide uptake, and adherence assay. In fungal keratitis (FK) mouse models, immunostaining was performed for investigating toll-like receptor 4 (TLR-4) expression and macrophage infiltration. Real-time PCR, ELISA, and Western blot were used to evaluate the expression of pro-inflammatory factors IL-1β, TNF-α, and IL-6 in infected RAW264.7 cells. Cells were also treated with TLR-4 siRNA or agonist CRX-527 to investigate mechanisms underlying the anti-inflammatory activity of quercetin. ResultsQuercetin at 32 μM was non-toxic to corneal epithelial and significantly inhibited A. fumigatus growth and adhesion, and also altered the structure and reduced the number of mycelia. Quercetin significantly reduced macrophage infiltration in the mouse cornea, and attenuated the expression of TLR-4 in the corneal epithelium and stroma of mice with keratitis caused by A. fumigatus. In RAW264.7 cells infected by A. fumigatus, quercetin downregulated TLR-4 along with pro-inflammatory factors IL-1β, TNF-α, and IL-6. RAW cells with TLR-4 knockdown had reduced expression of factors after A. fumigatus infection, which was decreased even further with quercetin treatment. In contrast, cells with CRX-527 had elevated inflammatory factors compared to control, which was significantly attenuated in the presence of quercetin. ConclusionQuercetin plays a protective role in mouse A. fumigatus keratitis by inhibiting fungal load, disrupting hyphae structure, macrophage infiltration, and suppressing inflammation response in macrophages via TLR-4 mediated signaling pathway.

Quercetin ameliorates nonalcoholic fatty liver disease (NAFLD) via the promotion of AMPK-mediated hepatic mitophagy

The global incidence of nonalcoholic fatty liver disease (NAFLD) has been surging in recent years, however, no drug is currently approved to treat this disease. Quercetin, a natural flavonoid abundant in plants and fruits, has been reported to alleviate NAFLD, however, the exact molecular mechanism remains unclear. This study aims to further elucidate its potential mechanism of action. The beneficial effects and the underlying mechanism of quercetin in alleviating NAFLD were explored both in vitro and in vivo, by employing chemical inhibitors of autophagosomes (3-methyladenine, 3-MA), autolysosomes (chloroquine, CQ), AMPK (Compound C, CC) and SIRT1 (selisistat, EX-527). The levels of intracellular lipids, reactive oxygen species, mitochondria function, autophagy, and mitophagy were assessed by fluorescent labeling and examined using flow cytometry or confocal microscopy. Key protein expressions of autophagy, mitophagy, and inflammation were also determined. In vivo, quercetin was shown to dose-dependently effectively alleviate NAFLD, but intraperitoneal injection of 3-MA could block the beneficial effects of quercetin on body weight, liver weight, serum ALT/AST, hepatic ROS and inflammation. In vitro, quercetin could reduce intracellular lipids (Nile Red staining) and ROS/DHE accumulation, which could be also blocked by 3-MA or CQ. Furthermore, we found that CC could abrogate the protective effects of quercetin on lipid and ROS accumulation in vitro. Also, CC abolished the proautophagic and anti-inflammatory effects of quercetin, as shown by western blot determination and Lyso-Tracker labeling. Importantly, mitophagy, a specific form of mitochondria-targeted autophagy, was enhanced by quercetin, as demonstrated by PINK1/Parkin protein variation and immunofluorescence colocalization of autophagosomes and mitochondria, which could also be blocked by the intervention of CC. This study demonstrates that quercetin prevents NAFLD through AMPK-mediated mitophagy and suggests that promoting mitophagy via an upregulation of AMPK may be a promising therapeutic strategy against NAFLD.

An insight into anticancer, antioxidant, antimicrobial, antidiabetic and anti-inflammatory effects of quercetin: a review.

Flavonoids are present naturally in many fruits and vegetables including onions, apples, tea, cabbage, cauliflower, berries and nuts which provide us with quercetin, a powerful natural antioxidant and cytotoxic compound. Due to antioxidant property, many nutraceuticals and cosmeceuticals products contain quercetin as a major ingredient nowadays. Current review enlightened sources and quercetin’s role as an antioxidant, antimicrobial, antidiabetic, anticancerous and anti-inflammatory agent in medical field during last 5 to 6 years. Literature search was systematically done using scientific for the published articles of quercetin. A total of 345 articles were reviewed, and it was observed that more than 40% of articles were about quercetin’s use as an antioxidant agent, more than 25% of studies were about its use as an anticancer agent, and articles on antimicrobial activity were more than 15%. 10% of the articles showed anti-inflamamatory effects of quercetin. Literature search also revealed that quercetin alone and its complexes with chitosan, metal ions and polymers possessed good antidiabetic properties. Thus, the review focuses on new therapeutic interventions and drug delivery system of quercetin in medical field for the benefit of mankind.

Quercetin ameliorates Aspergillus fumigatus keratitis by inhibiting fungal growth, toll-like receptors and inflammatory cytokines

PurposeTo investigate the antifungal and anti-inflammatory effects of quercetin on Aspergillus fumigatus (A. fumigatus) keratitis. MethodsHuman corneal epithelial cells (HCECs) and C57BL/6 mice were stimulated by A. fumigatus and treated with quercetin or dimethyl sulfoxide (DMSO) after infection. In HCECs, minimum inhibitory concentration (MIC) and cytotoxicity tests (CCK-8) were used to detect the antifungal effect and cytotoxicity of quercetin. In mice with A. fumigatuskeratitis, clinical score, plate counting and hematoxylin-eosin (HE) staining were performed to evaluate the effects of quercetin in vivo. Myeloperoxidase (MPO) assay and immunofluorescence staining were applied to assess neutrophil recruitment and infiltration. Real time PCR (RT-PCR), enzyme-linked immunosorbent assay (ELISA) and western blot were used to detect the mRNA and protein expressions of inflammatory mediators. ResultsCompared with DMSO control, quercetin (16–64 μM) significantly inhibited the growth of A. fumigatus in a concentration-dependent manner without affecting cell viability in HCECs. In corneas of mice with A. fumigatuskeratitis, quercetin decreased clinical score and fungal load, and reduced neutrophil recruitment and infiltration to the corneal stroma. Moreover, quercetin attenuated the expression of inflammatory mediators including toll-like receptor-4 (TLR-4), TLR-2, interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α) and high mobility group box 1 (HMGB1) in vitro and in vivo. ConclusionsOur study demonstrated that quercetin treatment can ameliorate A. fumigatus keratitis by inhibiting the growth of A. fumigatus, decreasing neutrophil recruitment and infiltration, and downregulating the productions of TLR-4, TLR-2, TNF-α, IL-1β and HMGB1, indicating quercetin is likely to become a potential therapeutic agent in FK treatment.

Anti-Inflammatory Effects of Quercetin on High-Glucose and Pro-Inflammatory Cytokine Challenged Vascular Endothelial Cell Metabolism.

ScopePro‐inflammatory stimuli such as hyperglycemia and cytokines have been shown to negatively affect endothelial cell functions. The aim of this study is to assess the potential of quercetin and its human metabolites to overcome the deleterious effects of hyperglycemic or inflammatory conditions on the vascular endothelium by modulating endothelial cell metabolism.Methods and resultsA metabolomics approach enabled identification and quantification of 27 human umbilical vein endothelial cell (HUVEC) metabolites. Treatment of HUVECs with high‐glucose concentrations causes significant increases in lactate and glutamate concentrations. Quercetin inhibits glucose‐induced increases in lactate and adenosine 5′‐triphosphate (ATP) and also increased inosine concentrations. Tumor necrosis factor α‐treatment (TNFα) of HUVECs causes increases in asparagine and decreases in aspartate concentrations. Co‐treatment with quercetin reduces pyruvate concentrations compared to TNFα‐only treated controls. Subsequently, it was shown that quercetin and its HUVEC phase‐2 conjugates inhibit adenosine deaminase, xanthine oxidase and 5′nucleotidase (CD73) but not ectonucleoside triphosphate diphosphohydrolase‐1 (CD39) or purine nucleoside phosphorylase activities.ConclusionQuercetin was shown to alter the balance of HUVEC metabolites towards a less inflamed phenotype, both alone and in the presence of pro‐inflammatory stimuli. These changes are consistent with the inhibition of particular enzymes involved in purine metabolism by quercetin and its HUVEC metabolites.

Quercetin Decreased Alveolar Bone Loss and Apoptosis in Experimentally Induced Periodontitis Model in Wistar Rats

Quercetin is a flavonoid which has potent anti-inflammatory, antibacterial, and antioxidant effect. Purpose of this study was to evaluate effects of quercetin on alveolar bone loss and histopathological changes in ligature-induced periodontitis in rats. Wistar rats were divided into four experimental groups: non-ligated control (C, n=8) group; periodontitis (P, n=8) group; ligature and low dose quercetin group (75 mg/kg/day quercetin, Q75 group, n=8); ligature and high dose quercetin group (150 mg/kg/day quercetin, Q150 group, n=8). Silk ligatures were placed at gingival margin of lower first molars of mandibular right quadrant. Study duration was 15 days, and animals were sacrificed end of this period. Changes in alveolar bone levels were clinically measured and tissues were immunohistochemically examined, matrix metalloproteinase 8 (MMP 8), inducible nitric oxide synthase (iNOS), tissue inhibitor of metalloproteinase 1 (TIMP 1), Cysteine-aspartic proteases 3 (Caspase 3), and tartrate-resistant acid phosphatase (TRAP) positive osteoclast cells, osteoblast, and neutrophil counts were also determined. Alveolar bone loss was highest in P group, and differences among P, Q75, and Q150 groups were significant. Both doses of quercetin decreased TRAP+ osteoclast cells and increased osteoblast cells. Inflammation in P group was also higher than those of C, Q75, and Q150 groups indicating anti-inflammatory effect of quercetin. iNOS, MMP-8, and caspase-3 levels were highest, and TIMP-1 expression was lowest in P group; differences were statistically significant. Within limits of this study, it can be suggested that quercetin administration may reduce alveolar bone loss by increasing osteoblastic activity, decreasing osteoclastic activity, apoptosis, and inflammation in an experimental model of periodontitis.

Biochemical Evaluation of the Effects of Quercetin On Experimental Acute Methanol Intoxication in Rats

Previous studies have shown the role of oxidative stress in methanol toxicity. Also, studies have shown antioxidant, anti-inflammatory effects of quercetin (Q). This study evaluates the effect of quercetin (Q) administration on total oxidant status (TOS), total anti-oxidant status (TAS), oxidative stress index (OSI) and paraoxanase 1 (PON1) levels in rats with experimentally-induced methanol (MeOH) intoxication. Six groups were constituted as control, methotrexate (Mtx), Mtx+MeOH, Mtx+MeOH+ethanol (EtOH), Mtx+MeOH+Q1, Mtx+MeOH+Q2. All rats except controls were injected Mtx (0.3 mg/kg daily) intra-peritoneally (IP) for 7 days. On the 8th day of the test, 3 g/kg MeOH was injected IP in MeOH, EtOH and Q groups. Four hours after MeOH administration, 0.5 g/kg EtOH was injected IP in EtOH group and 50 mg/kg Q was administered IP in Q1 and Q2 groups. In addition, a total of 5 doses of 50 mg/kg Q was injected IP 24, 48, 72 and 96 hours after the first dose in Q2 group. Saline solution was given IP in the other groups. Rats were sacrificed with anesthesia 8 hours after the administrations. Blood samples were obtained for evaluating total oxidant status (TOS), total anti-oxidant status (TAS), oxidative stress index (OSI) and paraoxanase 1 (PON1) levels. The highest TOS level was found in MeOH+MTx group. A significant reduction was detected in serum TOS levels in MeOH+Mtx+EtOH, MeOH+Mtx+Q1 and MeOH+Mtx+Q2 groups. The lowest serum TAS level was detected in MeOH+Mtx group. Maximum TAS level elevation was found in MeOH+Mtx+Q2, MeOH+Mtx+Q1 and MeOH+Mtx+EtOH groups. The highest OSI ratio was found in MeOH+Mtx group. A reduction was detected in OSI ratios in MeOH+Mtx+EtOH, MeOH+Mtx+Q1 and MeOH+Mtx+Q2 groups as compared to MeOH+Mtx group. The lowest serum PON1 level was found in MeOH+Mtx group. Maximum serum PON1 level elevation was found in MeOH+Mtx+Q2 group. The results indicating that quercetin administration could be effective on both acute and subacute processes of methanol intoxication were tried to be revealed through serum TOS, TAS, OSI and PON1 levels. These results show that quercetin could be used as an alternative treatment option in methanol intoxication.

Modulation of Chronic Inflammation by Quercetin: The Beneficial Effects on Obesity.

Obesity has become a major risk factor for the development of chronic diseases such as insulin resistance, type 2 diabetes mellitus, and cardiovascular disease. Moreover, obesity induces chronic inflammation in adipose tissue, liver, skeletal muscle, and the vascular system. Quercetin is the major representative of the flavonoid subclass of flavonols, which is ubiquitously contained within natural plants such as green tea, and vegetables, including onions and apples. Researchers have focused greater attention to the beneficial physiological roles of quercetin, which has anti-oxidative, anti-inflammatory, and anti-fibrotic effects on insulin resistance and atherosclerosis in obesity-related diseases. Also, the anti-inflammatory effects of quercetin on intestinal microbiota have been demonstrated in obesity. In addition, there is increasing evidence that quercetin is associated with epigenetic activities in cancer, and in maternal undernutrition during gestation and lactation. In this review, we focus on the chemical properties of quercetin, its dietary sources in obesity, and its anti-inflammatory effects on insulin resistance, atherosclerosis, intestinal microbiota, and maternal under-nutrition with epigenetic activity.

Quercetin Promotes Diabetic Wound Healing via Switching Macrophages From M1 to M2 Polarization

BackgroundFor patients with diabetes mellitus, excessive and long-lasting inflammatory reactions at the wound site commonly lead to the delayed refractory wound healing. The polarization of macrophages in terms of M1 and M2 phenotypes is closely related to the production of inflammatory cytokines. Quercetin is traditionally recognized to have anti-inflammatory effect; however, whether quercetin modulates macrophage polarization from M1 to M2 and thus promotes diabetic wound healing remain unknown. Materials and methodsWounded male diabetic rats were equally divided into five groups: model group, solvent control group (10% DMSO), and three drug groups treated with quercetin (Q) at concentrations of 10 mg/mL (Q-LD [low dose]), 20 mg/mL (Q-MD [medium dose]), and 40 mg/mL (Q-HD [high dose]), respectively. The anti-inflammatory effect of quercetin on diabetic wounds was observed. Immunohistochemistry and quantificational real-time polymerase chain reaction were applied to test the changes in macrophage polarization and inflammatory responses. ResultsThe wound contraction was fastest in Q-HD group. Hematoxylin and eosin (H&E) and Masson's trichrome staining revealed that fibroblast distribution and collagen deposition in quercetin-treated groups were significantly higher than those in the model group. Immunohistochemistry tests showed more CD206-positive cells and less iNOS-positive cells in quercetin-treated groups. Furthermore, the levels of proinflammatory factors in quercetin-treated groups were lower than those in the model group, whereas the levels of the anti-inflammatory factors and angiogenesis-related factors were relatively higher. ConclusionsIn short, quercetin inhibits inflammatory reactions via modulating macrophage polarization switching from M1 to M2 phenotype, thereby accelerating the diabetic wound repair.

Anti-inflammatory effects of quercetin in a mouse model of MC903-induced atopic dermatitis

In this study, the anti-inflammatory mechanisms of Quercetin (Que) on atopic dermatitis (AD)-like skin lesions was examined. The left ear of mice was applied with MC903, followed by Que. administration daily on the ear for 8 days. Then macroscopic and histologic examination was performed to detect the severity of skin lesions. In the skin section of AD mice, we observed that Que. could reduce the expression of CCL17, CCL22, IL-4, IL-6, IFN-γ and TNF-α. In vitro, the anti-inflammatory effects of Que. were examined on human keratinocytes (HaCaT cells) treated with IFN-γ/TNF-α. To unveil the lncRNAs' regulatory role on Que-activated anti-inflammatory function, the next-generation high-throughput sequencing was performed in HaCat cells with or without Que. treatment, which profiled the expression of lncRNAs and mRNAs, the results illustrated that lnc-C7orf30–2, a lncRNA expressed differentially, was correlated with IL-6 expression. Silencing of lnc-C7orf30–2 by RiboTM lncRNA Smart Silencer proved its role on IL-6 expression. Therefore, the results here demonstrated that topical administration of Que. plays a beneficial role in controlling AD symptoms, which may serve as potential candidate for AD treatment.

Topical Quercetin and Resveratrol Protect the Ocular Surface in Experimental Dry Eye Disease

ABSTRACTPurpose: To determine the anti-inflammatory effect of quercetin (QCT), resveratrol (RES), and their combination in a dry eye disease (DED) model.Methods: 0.01% QCT, 0.1% RES, 0.01% QCT + 0.1% RES (QCT + RES) or vehicle were topically applied in a desiccating stress (DS) mice model. CD4+ T cells isolated from DS-exposed mice were transferred to athymic recipient mice. Corneal fluorescein staining, tear production, and tear cytokine levels were evaluated in DS-exposed mice, and conjunctival CD4+ T cell infiltration was evaluated in recipient mice.Results: QCT (p < 0.001) and QCT + RES (p < 0.05) reduced corneal staining in DS-exposed mice. IL-1α tear concentration was reduced by QCT, RES, and QCT + RES (p < 0.05, 0.01 and 0.01, respectively) compared to DS + vehicle mice. CD4+ T cells increased in recipients of DS-exposed mice (p < 0.05) and were lower in recipients of QCT- and RES-treated mice (p < 0.05).Conclusion: The anti-inflammatory effect of QCT, RES, and QCT + RES on DED-experimental model suggests that their topical application could be used for DED treatment.

The Effects of Raw Red Onion Consumption on Serum Levels of Adiponectin, Leptin, and hs-CRP in Overweight/Obese Females with Polycystic Ovarian Syndrome: A Randomized Controlled-Clinical Trial

Background: Chronic low-grade inflammation has been confirmed to be a major etiological factor in polycystic ovarian syndrome (PCOS). The anti-inflammatory effects of quercetin, a major flavonol in onion, have been suggested by experimental studies. However, lack of data exists to investigate the effects of onion on inflammatory markers in PCOS. Objectives: This study aimed at assessing the effects of raw red onion consumption on inflammatory markers in PCOS. Methods: Fifty-four overweight/obese patients with PCOS were randomly assigned to either High-Onion (HO; raw red onions: 2 (40 - 50 g/day) for overweight and 2 (50 - 60 g/day) for obese patients) or Low-Onion (LO; raw red onions: 2 (10 - 15 g/day)) group over 8 weeks in this randomized controlled trial (RCT). Serum adiponectin, leptin, and high-sensitivity C-reactive protein (hs-CRP) levels and their correlations with metabolic and anthropometric parameters were assessed at baseline and endpoint. Results: The 2-month treatment with onion could not significantly effect mean serum levels of adiponectin, leptin, or hs-CRP. However, the percentage change of serum adiponectin was significantly different between the two groups after 8 weeks (-11.9% in LO vs. 48.32% in HO; P = 0.026). Percentage change of serum leptin and hs-CRP showed no significant differences between the 2 groups. Leptin had significant correlations with most anthropometric and metabolic variables of insulin resistance (P < 0.05). Adiponectin concentration correlated significantly with fasting glucose (r = -0.35; P < 0.05), while log hs-CRP had significant correlations with most of the anthropometric markers (P < 0.05). Conclusions: The 8-week intervention with red onion could increase percentage changes of serum adiponectin level in overweight/obese females with PCOS. However, no such effect was observed for serum leptin as well as hs-CRP levels.

Anti-inflammatory Effects of Quercetin and Vitexin on Activated Human Peripheral Blood Neutrophils: - The effects of quercetin and vitexin on human neutrophils.

ObjectivesPolymorphonuclear neutrophils (PMNs) constitute the first line of defense against invading microbial pathogens. Early events in inflammation involve the recruitment of neutrophils to the site of injury or damage where changes in intracellular calcium can cause the activation of pro-inflammatory mediators from neutrophils including superoxide generation, degranulation and release of myeloperoxidase (MPO), productions of interleukin (IL)-8 and tumor necrosis factor α (TNF-α), and adhesion to the vascular endothelium. To address the anti-inflammatory role of flavonoids, in the present study, we investigated the effects of the flavonoids quercetin and vitexin on the stimulus-induced nitric oxide (NO), TNF-α, and MPO productions in human neutrophils.MethodsHuman peripheral blood neutrophils were isolated, and their viabilities were determined by using the Trypan Blue exclusion test. The polymorphonuclear leukocyte (PMNL) preparations contained more than 98% neutrophils as determined by morphological examination with Giemsa staining. The viabilities of cultured neutrophils with various concentrations of quercetin and vitexin (1 – 100 μM) were studied using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assays. Neutrophils were cultured in complete Roswell Park Memorial Institute (RPMI) medium, pre-incubated with or without quercetin and vitexin (25 μM) for 45 min, and stimulated with phorbol 12-myristate 13-acetate (PMA) (10−7 M). NO production was carried out through nitrite determination by using the Griess method. Also, the TNF-α and the MPO productions were measured using enzyme-linked immunosorbent assay (ELISA) kits and MPO assay kits.ResultsNeutrophil viability was not affected up to a concentration of 100 μM of quercetin or vitexin. Both quercetin and vitexin significantly inhibited TNF-α, NO, and MPO productions in human neutrophils (P < 0.001).ConclusionThe present study showed that both quercetin and vitexin had significant anti-inflammatory effects. Thus, treatment with either quercetin or vitexin may be considered as a therapeutic strategy for treating patients with neutrophil-mediated inflammatory diseases.

Anti-Inflammatory Effect of Quercetin on RAW 264.7 Mouse Macrophages Induced with Polyinosinic-Polycytidylic Acid.

Quercetin (3,3′,4′,5,6-pentahydroxyflavone) is a well-known antioxidant and a flavonol found in many fruits, leaves, and vegetables. Quercetin also has known anti-inflammatory effects on lipopolysaccharide-induced macrophages. However, the effects of quercetin on virus-induced macrophages have not been fully reported. In this study, the anti-inflammatory effect of quercetin on double-stranded RNA (dsRNA)-induced macrophages was examined. Quercetin at concentrations up to 50 μM significantly inhibited the production of NO, IL-6, MCP-1, IP-10, RANTES, GM-CSF, G-CSF, TNF-α, LIF, LIX, and VEGF as well as calcium release in dsRNA (50 µg/mL of polyinosinic-polycytidylic acid)-induced RAW 264.7 mouse macrophages (p < 0.05). Quercetin at concentrations up to 50 μM also significantly inhibited mRNA expression of signal transducer and activated transcription 1 (STAT1) and STAT3 in dsRNA-induced RAW 264.7 cells (p < 0.05). In conclusion, quercetin had alleviating effects on viral inflammation based on inhibition of NO, cytokines, chemokines, and growth factors in dsRNA-induced macrophages via the calcium-STAT pathway.

C4-P-06Anti-diabetic and Anti-Inflammatory Effects of Quercetin in Streptozocin-Induced Diabetic Rats

C4-P-06Anti-diabetic and Anti-Inflammatory Effects of Quercetin in Streptozocin-Induced Diabetic Rats

A Two-Week Quercetin Supplementation in Horses Results in Moderate Accumulation of Plasma Flavonol Concentrations

Quercetin is a plant-derived flavonoid with strong anti-inflammatory properties. Previously, systemic availability of quercetin was documented in horses. We investigated effects of a daily quercetin supplementation on plasma concentrations of quercetin and its metabolites over two weeks. Additionally, plasma concentrations of selected proinflammatory and anti-inflammatory cytokines were analyzed before and immediately after the experiment. Four adult Warmblood horses with a mean body weight ± standard error of the mean of 551 ± 46 kg were used. During a two-week pre-experimental phase and also during the experiment, the use of dietary supplements, apples, or any form of medication was excluded; the horses were offered hay ad libitum, concentrated feed individually (7 AM and PM), and 8 hours access to pasture. During the experiment, quercetin (10 mg/kg body weight) was administrated within the evening meals. Blood samples were collected (jugular vein) three times during the pre-experimental phase and on days 4, 8, 11, and 14 after the start of the experiment. Flavonols in plasma and feed were analyzed by high-performance liquid chromatography; plasma concentrations of cytokines were measured using commercial enzyme-linked immunosorbent assay kits. Daily quercetin supplementations for two weeks increased kaempferol and thus total plasma flavonol concentrations time dependently without accumulation of quercetin or its methylated metabolite isorhamnetin. Although proinflammatory cytokines stayed below detection limit, plasma concentrations of anti-inflammatory cytokines (interleukin-10, interleukin-1 receptor antagonist) were enhanced by quercetin feeding. The study indicates that dietary quercetin supplementation moderately induces total plasma flavonols and thus may be useful in controlling inflammatory disorders in horses. However, anti-inflammatory effects of quercetin must be confirmed in controlled trials.

Anti-inflammatory effects of Quercetin and Epigallocatechin gallate in human primary bronchial epithelial cells

Anti-inflammatory effects of Quercetin and Epigallocatechin gallate in human primary bronchial epithelial cells