Anti-inflammatory effect of quercetin-loaded microemulsion in the airways allergic inflammatory model in mice

Rogério, Alexandre de Paula; Dora, Cristiana Lima; Andrade, Edinéia Lemos de; Chaves, J.; Silva, Luis F.C.; Lemos‐Senna, Elenara; Calixto, João B.

doi:10.1016/j.phrs.2009.10.005

Cited by 172 publications

(88 citation statements)

References 46 publications

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“…Recently, quercetin has been detected as an inhibitor of interleukin 1 beta (IL-1β) induced intercellular adhesion molecule-1 (ICAM-1) expression and nuclearfactor-kappa B (NF-κB) activity in human A549 lung cells [15]. Indeed oral administration of quercetin in animal models was reported to inhibit experimentally induced pulmonary fibrosis, [16] airway inflammation [17] and emphysema [18]. Mi et al [19] showed that quercetin suppressed oxidative damage characterized by lipid peroxidation, decreased spermatogonial cell numbers, vacuolated cytoplasm and condensed nuclei in spermatogonial cells of embryonic chicken exposed to 3-methyl-4-nitrophenol.…”

Section: Introductionmentioning

confidence: 99%

The possible protective role of quercetin on induced cardiac Oxidative DNA Damage by repeated exposure to diesel exhaust nanoparticles in rats (a histological and immunohistochemical study)

Faruk¹,

Mansy²,

ALasmari³

et al. 2018

J Histol Histopathol

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Diesel exhaust nanoparticles (DENPs) are gaseous exhaust and one component of particulate matter (PM) air pollution which is found to cause health hazards in humans. Quercetin is widely known for its antioxidant and antitoxic potential. We aimed todetect the protective effect of quercetin in DENP-induced cardio toxicity. Fifty Malealbino rats were divided into two groups,first group (ten rats) divided into two equal subgroups (one receive saline act as control and other receive quercetin,the second group (forty rats)divided equally into two subgroups (one was treated with repeated doses of DENPs [90µg/ rat and 180µg/ rat for 6 days intratracheally every two days] and other treated orally with quercetin (60 mg/kg B.Wt.) 1h prior to DENP exposure,DNA damagewas examined by measureserum8-hydroxydeoguanosine (8-OHdG) levels followed by histological and immunohistochemical studies for nuclear factor-kappa B(NF-κB) expression in heart tissues. Tumor necrosis factor-alpha (TNFα), interleukin-6 (IL-6) and serum level 8-Ohd Gare significantly higher in repeated doses of DENPs than the control group. Pretreatment with quercetin reduced significantly serum level 8-OhdGwhen compared to DENPs group.Cardiac myocytes disruption, vacuolation, inflammation and wide separation of its fibers in contrast to control group. Myocyteinflammations were significantly decreased with quercetin group compared with control group (decrease NF-κBimmunostaining). The present work yields experimentalevidence that quercetin can reduce oxidative DNA damage and inflammation induced by DENPs, so suggested that quercetin possible cardioprotective effect against DENPs.

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Section: Introductionmentioning

confidence: 99%

The possible protective role of quercetin on induced cardiac Oxidative DNA Damage by repeated exposure to diesel exhaust nanoparticles in rats (a histological and immunohistochemical study)

Faruk¹,

Mansy²,

ALasmari³

et al. 2018

J Histol Histopathol

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“…In another recent report by Lisi et al (2011) quercetin was shown to reduce cell proliferation and hyaluronan production. Quercetin has been shown to exhibit antioxidant, anti-inflammatory, and antiadipogenic properties in other cell systems and animal models (Comalada et al 2005, Rotelli et al 2009, Vasquez-Garzon et al 2009, Ying et al 2009, Rogerio et al 2010. Here, we investigated the anti-adipogenic role of quercetin in OFs stimulated by oxidants, such as CSE and H 2 O 2 , as well as associations between the anti-adipogenic and antioxidant effects of quercetin, including its reduction of ROS production.…”

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confidence: 99%

Cigarette smoke extract-induced adipogenesis in Graves' orbital fibroblasts is inhibited by quercetin via reduction in oxidative stress

Yoon¹,

Lee²,

Chae³

et al. 2012

Journal of Endocrinology

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Cigarette smoking is known to aggravate Graves' orbitopathy (GO) severity by enhancing adipogenesis. We investigated the effect of quercetin, an antioxidant, on adipocyte differentiation induced by cigarette smoke extract (CSE) in primary cultured orbital fibroblasts (OFs) from GO patients. Freshly prepared CSE was added to the cells and H 2 O 2 was used as a positive control. Intracellular reactive oxygen species (ROS) generation and adipogenesis were measured. The expressions of proteins peroxisome proliferator-activated receptor (PPAR) g, CCAAT-enhancer-binding proteins (C/EBP) a and b, and heme oxygenase-1 (HO-1), an antioxidant enzyme, were examined during adipogenic differentiation. In result, CSE and H 2 O 2 dose-dependently stimulated intracellular ROS production in normal and Graves' OFs. The effect of 2% CSE was similar to that of 10 mM H 2 O 2 ; both concentrations were noncytotoxic and were used throughout the experiment. Quercetin pretreatment reduced the ROS generation stimulated by either CSE or H 2 O 2 in preadipocyte OFs. CSE and H 2 O 2 stimulated adipocyte differentiation in cultured OFs. The addition of quercetin (50 or 100 mM) suppressed adipogenesis. Quercetin also suppressed ROS generation in differentiating OFs during adipogenesis stimulated by CSE and H 2 O 2 . Additionally, the expressions of PPARg, C/EBPa, and C/EBPb proteins were reduced in the quercetin-treated OFs. Quercetin also reduced the CSE-and H 2 O 2 -induced upregulation of ROS and HO-1 protein in differentiated OFs and preadipocyte OFs. As shown in this study, quercetin inhibited adipogenesis by reducing ROS in vitro, supporting the use of quercetin in the treatment of GO. IntroductionOxidative stress is implicated in the pathogenesis of Graves' orbitopathy (GO), and cigarette smoking is known to be a major environmental factor that affects GO. Cigarette smoking has been shown to influence the incidence, severity, and responses to treatment of GO, and appears to do so in a dose-dependent and temporal manner. Reportedly, smokers with Graves' disease are approximately five times more likely to develop GO than Journal of Endocrinology Research J S YOON, H J LEE and othersTreatment of GO by quercetin, an antioxidant 216:2 145-156

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“…The antioxidant, free radical-scavenging, and neuroprotective effects of quercetin is well known (15)(16)(17) . Besides these important benefits of quercetin, it also has a protective effect against apoptotic cell damage.…”

Section: Discussionmentioning

confidence: 99%

Quercetin protects the retina by reducing apoptosis due to ischemia-reperfusion injury in a rat model

Arıkan¹,

Erşan²,

Karaca³

et al. 2015

Arquivos Brasileiros De Oftalmologia

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Purpose: This study aimed to investigate the effect of quercetin on apoptotic cell death induced by ischemia-reperfusion (I/R) injury in the rat retina. Methods: Twenty-four rats were divided into four equal groups: control, ischemic, solvent, and quercetin. I/R injury was achieved by elevating the intraocular pressure above the perfusion pressure. Intraperitoneal injections of 20 mg/kg of quercetin and dimethyl sulfoxide (DMSO) were performed in the quercetin and solvent groups, respectively, immediately prior to I/R injury, and the researchers allowed for the retinas to be reperfused. Forty-eight hours after injury, the thicknesses of the retinal ganglion cell layer (RGCL), inner nuclear layer (INL), inner plexiform layer (IPL), outer plexiform layer (OPL), and outer nuclear layer (ONL) were measured in all groups. Moreover, the numbers of terminal deoxynucleotidyl transferase dUTP nick-end-labeled [TUNEL (+)] cells and caspase-3 (+) cells in both INL and ONL were evaluated in all groups. Results: The administration of quercetin was found to reduce the thinning of all retinal layers. The mean thickness of INL in the quercetin and ischemic groups was 21 ± 5.6 µm and 16 ± 6.4 µm, respectively (P<0.05). Similarly, the mean thickness of ONL in the quercetin and ischemic groups was 50 ± 12.8 µm and 40 ± 8.7 µm, respectively (P<0.05). The antiapoptotic effect of quercetin in terms of reducing the numbers of both TUNEL (+) cells and caspase-3 (+) cells was significant in INL. The mean number of TUNEL (+) cells in INL in the ischemic and quercetin groups was 476.8 ± 45.6/mm 2 and 238.72 ± 251/mm², respectively (P<0.005). The mean number of caspase-3 (+) cells in INL of ischemic and quercetin groups was 633.6 ± 38.7/mm 2 and 342.4 ± 36.1/mm 2 , respectively (P<0.001). Conclusion:The use of quercetin may be beneficial in the treatment of retinal I/R injury because of its antiapoptotic effect on the retinal layers, particularly in INL.

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Anti-inflammatory effect of quercetin-loaded microemulsion in the airways allergic inflammatory model in mice

Cited by 172 publications

References 46 publications

The possible protective role of quercetin on induced cardiac Oxidative DNA Damage by repeated exposure to diesel exhaust nanoparticles in rats (a histological and immunohistochemical study)

The possible protective role of quercetin on induced cardiac Oxidative DNA Damage by repeated exposure to diesel exhaust nanoparticles in rats (a histological and immunohistochemical study)

Cigarette smoke extract-induced adipogenesis in Graves' orbital fibroblasts is inhibited by quercetin via reduction in oxidative stress

Quercetin protects the retina by reducing apoptosis due to ischemia-reperfusion injury in a rat model

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