Beneficial Effects Of Quercetin Research Articles

P37 | Beneficial effect of quercetin, 3‐o‐methylquercetin and rhamnazin in lipopolysaccharide‐induced inflammation in porcine intestinal cells

Journal of Veterinary Pharmacology and TherapeuticsVolume 46, Issue S1 p. 103-103 POSTER PRESENTATIONS P37 | Beneficial effect of quercetin, 3-o-methylquercetin and rhamnazin in lipopolysaccharide-induced inflammation in porcine intestinal cells First published: 11 June 2023 https://doi.org/10.1111/jvp.13316Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL No abstract is available for this article. Volume46, IssueS1Special Issue: 15th International Congress of the European Association for Veterinary Pharmacology and Toxicology held Bruges, Belgium, July 2–5, 2023June 2023Pages 103-103 RelatedInformation

Beneficial effects of quercetin on vincristine-induced liver injury in rats: Modulating the levels of Nrf2/HO-1, NF-kB/STAT3, and SIRT1/PGC-1α.

Our experimental objective was to investigate the hepatotoxic effect of vincristine (VCR) administration in rats and determined whether combined therapy with Quercetin (Quer) ensured protection. Five groups with seven rats each were used for this purpose, and experimental groups were formulated as follows: Control group; Quer group; VCR group; VCR plus Quer 25 group; VCR plus Quer 50 group. The results showed that VCR significantly increased the activity of alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP) enzymes. Besides, VCR caused considerable increases in the malondialdehyde (MDA) contents, along with significant decreases in reduced glutathione levels, superoxide dismutase, catalase, and glutathione peroxidase enzyme activities in the rat livers. Quer treatment in VCR toxicity markedly decreased the activity of ALT, AST, ALP enzymes, and MDA contents and enhanced the activities of antioxidant enzymes. The results also showed that VCR significantly increased the levels of NF-kB, STAT3, and the expression of caspase 3, Bax, and MAP LC3 and decreased the expression of Bcl2 and levels of Nrf2, HO-1, SIRT1, and PGC-1α. Compared to the VCR group, Quer treatment exhibited significantly lower levels of NF-kB, STAT3, and the expression of caspase 3, Bax, and MAP LC3, and higher levels of Nrf2, HO-1, SIRT1, and PGC-1α. In conclusion, our study demonstrated that Quer could alleviate the harmful effects of VCR via activation of NRf2/HO-1 and SIRT1/PGC-1α pathways, and via attenuation of oxidative stress, apoptosis, autophagy, and NF-kB/STAT3 pathways.

Use of agricultural production waste in relation to bio nano technology for the synthesis of functionalized selenium nanoparticles

The application of nanotechnological innovations to increase the effectiveness of the bioflavonoid quercetin is considered. The ability to functionalize with specific ligands that target specific organs or cells is very important because it is possible to increase the concentration of quercetin at the desired target level while reducing side effects. Quercetin, as a flavonoid antioxidant, is widely used to reduce oxidative stress and activate important signalling pathways in cells. However, poor solubility in water, intensive first-pass metabolism limits its use. A strategy for the development of nanocomposites is presented, which involves combining quercetin obtained from agricultural waste with selenium nanoparticles. In vitro results demonstrated that quercetin-nanoselenium has high water solubility compared to individual flavonoids. It has been proven that quercetin-nano-selenium nanoparticles are capable of reducing 1,1-dipheny l-2-picrylhydrazyl (DPPH) radicals and are characterized by high antioxidant activity. The ability to functionalize nanoparticles with specific ligands that target the modulation of specific signaling pathways (Keap1/ Nrf2/ARE, Nf-kB, mTOR) in individual cells is very important, as it allows increasing the concentration of quercetin to the desired level while reducing side effects. Considering the beneficial effects of quercetin, a strategy has been developed that involves the use of selenium nanoparticles to deliver quercetin in a specific and controlled manner. Research in this direction is promising, as it will contribute to clarifying the expediency of using such nanosystems, which have not yet been widely used. The use of onion waste and its extracts in biotechnology, biomedicine, pharmaceuticals and the agro-industrial sector can be an optimal solution for reducing environmental damage. In addition, it will provide an economically determined alternative for the production of feed additives for animals and poultry. Compounds of quercetin with nanoselenium should take a worthy place in clinical medical practice, biology and agriculture. The beneficial effects of quercetin can be further enhanced with the help of nanotechnology, which will contribute to the effective use of this compound with such great biological potential. Key words: nanobiotechnologies, waste, onion peel, 1,1-dipheny l- 2-picrylhydrazyl, antiradical activity.

Hepatic transcriptome profiles reveal the hepatoprotective effects of dietary quercetin and sodium quercetin-5′-sulfonates supplementation in hybrid grouper (Epinephelus fuscoguttatus♀ × Epinephelus polyphekadion♂)

Plant flavonoids, such as quercetin (QE), are traditionally used to treat liver injuries. Given the limited bioavailability of quercetin, sodium quercetin-5′-sulfonates (QS) were synthesised and characterised. Although beneficial effects of QE on the fatty liver are observed in vertebrates, the exact mechanism is still unclear, particularly in fish livers. As a result, RNA-sequencing was conducted on hepatic libraries from hybrid groupers (Epinephelus fuscoguttatus♀ × Epinephelus polyphekadion♂) after QE and QS exposure for 56 d. In total, 49,411 unigenes were generated with a control group (FM, 0 mmol/kg), QE (QE, 3.2 mmol/kg), and QS (QS, 3.2 mmol/kg) supplementation group. The N50 for the unigenes is 2047 bp, whereas the mean length is 1198.55 bp. Compared with FM, we identified 788 and 848 differentially expressed unigenes (DEGs) in the liver in response to QE and QS, including 423 up- and 365 down-regulated in the QE group and 402 up- and 446 down-regulated in the QS group. Furthermore, ten genes were selected for real-time quantitative PCR to verify the reliability of our transcriptome data, and the result has shown that both up-and down-regulated genes were consistent with the RNA-seq results. Results showed that QE down-regulated hepatic genes involved in the steroid biosynthesis pathway, while QS up-regulated genes related to polyamine synthesis. More importantly, glutaminase1 (GLS1) is the initial and rate-limiting enzyme responsible for glutamine catabolism, down-regulated by QE and QS exposure. Our results will provide valuable information to help understand the underlying molecular mechanism for QE and QS preventing fatty liver of grouper.

Beneficial Effects of Quercetin on Microcystin-LR Induced Tight Junction Defects.

Quercetin has numerous functions including antioxidant and anti-inflammatory effects. The beneficial effect of quercetin against microcystin-LR (MC-LR)-induced testicular tight junctions (TJs) defects in vitro and in vivo were investigated. Significant reductions in transepithelial electrical resistance, occludin, and zonula occludens-1(ZO-1) levels were detected in the MC-LR-treated TM4 cells, and quercetin attenuated these effects. Interestingly, quercetin suppressed MC-LR-induced phosphorylation of protein kinase B (AKT). It effectively inhibited the accumulation of reactive oxygen species (ROS) in cells stimulated by MC-LR. In addition, ROS inhibitors blocked the TJ damage that is dependent on the AKT signaling pathway induced by MC-LR. In conclusion, our results suggest that alleviates MC-LR-impaired TJs by suppressing the ROS-regulated activation of the AKT pathway.

Low dose of quercetin-loaded pectin/casein microparticles reduces the oxidative stress in arthritic rats

AimsQuercetin has been investigated as an agent to treat rheumatoid arthritis. At high doses it improves inflammation and the antioxidant status of arthritic rats, but it also exerts mitochondriotoxic and pro-oxidant activities. Beneficial effects of quercetin have not been found at low doses because of its chemical instability and low bioavailability. In the hope of overcoming these problems this study investigated the effects of long-term administration of quercetin-loaded pectin/casein microparticles on the oxidative status of liver and brain of rats with adjuvant-induced arthritis. Main methodsParticle morphology was viewed with transmission electron microscopy and the encapsulation efficiency was measured indirectly by X-ray diffraction. Quercetin microcapsules (10 mg/Kg) were orally administered to rats during 60 days. Inflammation indicators and oxidative stress markers were measured in addition to the respiratory activity and ROS production in isolated mitochondria. Key findingsQuercetin was efficiently encapsulated inside the polymeric matrix, forming a solid amorphous solution. The administration of quercetin microparticles to arthritic rats almost normalized protein carbonylation, lipid peroxidation, the levels of reactive oxygen species as well as the reduced glutathione content in both liver and brain. The paw edema in arthritic rats was not responsive, but the plasmatic activity of ALT and the mitochondrial respiration were not affected by quercetin, indicating absence of mitochondriotoxic or hepatotoxic actions. SignificanceQuercetin-loaded pectin/casein microcapsules orally administered at a low dose improve oxidative stress of arthritic rats without a strong anti-inflammatory activity. This supports the long-term use of quercetin as an antioxidant agent to treat rheumatoid arthritis.

Beneficial Effect of Quercetin on Erythrocyte Properties in Type 2 Diabetic Rats.

Diabetes mellitus is characterized by tissue oxidative damage and impaired microcirculation, as well as worsened erythrocyte properties. Measurements of erythrocyte deformability together with determination of nitric oxide (NO) production and osmotic resistance were used for the characterization of erythrocyte functionality in lean (control) and obese Zucker diabetic fatty (ZDF) rats of two age categories. Obese ZDF rats correspond to prediabetic (younger) and diabetic (older) animals. As antioxidants were suggested to protect erythrocytes, we also investigated the potential effect of quercetin (20 mg/kg/day for 6 weeks). Erythrocyte deformability was determined by the filtration method and NO production using DAF-2DA fluorescence. For erythrocyte osmotic resistance, we used hemolytic assay. Erythrocyte deformability and NO production deteriorated during aging—both were lower in older ZDF rats than in younger ones. Three-way ANOVA indicates improved erythrocyte deformability after quercetin treatment in older obese ZDF rats only, as it was not modified or deteriorated in both (lean and obese) younger and older lean animals. NO production by erythrocytes increased post treatment in all experimental groups. Our study indicates the potential benefit of quercetin treatment on erythrocyte properties in condition of diabetes mellitus. In addition, our results suggest potential age-dependency of quercetin effects in diabetes that deserve additional research.

The Effect of Exogenous Application of Quercetin Derivative Solutions on the Course of Physiological and Biochemical Processes in Wheat Seedlings.

Quercetin, classified as a flavonoid, is a strong antioxidant that plays a significant role in the regulation of physiological processes in plants, which is particularly important in the case of biotic and abiotic stresses. The study investigated the effect of the use of potassium quercetin solutions in various concentrations (0.5%, 1.0%, 3.0% and 5.0%) on the physiological and biochemical properties of wheat seedlings. A pot experiment was carried out in order to determine the most beneficial dose of this flavonoid acting as a bio-stimulant for wheat plants. Spraying with quercetin derivative solutions was performed twice, and physiological measurements (chlorophyll content and fluorescence as well as gas exchange) were carried out on the first and seventh days after each application. The total phenolic compounds content and the total antioxidant capacity were also determined. It was shown that the concentrations of potassium quercetin applied have a stimulating effect on the course of physiological processes. In the case of most of the tested physiological parameters (chlorophyll content and fluorescence and gas exchange) and the total antioxidant capacity, no significant differences were observed in their increase as a result of application with concentrations of 3.0 and 5.0%. Therefore, the beneficial effect of quercetin on the analysed parameters is already observed when spraying with a concentration of 3.0%.

Quercetin Attenuates Trauma-Induced Heterotopic Ossification by Tuning Immune Cell Infiltration and Related Inflammatory Insult.

Heterotopic ossification (HO) is one of the most intractable disorders following musculoskeletal injury and is characterized by the ectopic presence of bone tissue in the soft tissue leading to severe loss of function in the extremities. Recent studies have indicated that immune cell infiltration and inflammation are involved in aberrant bone formation. In this study, we found increased monocyte/macrophage and mast cell accumulation during early HO progression. Macrophage depletion by clodronate liposomes and mast cell stabilization by cromolyn sodium significantly impeded HO formation. Therefore, we proposed that the dietary phytochemical quercetin could also suppress immune cell recruitment and related inflammatory responses to prevent HO. As expected, quercetin inhibited the monocyte-to-macrophage transition, macrophage polarization, and mast cell activation in vitro in a dose-dependent manner. Using a murine burn/tenotomy model, we also demonstrated that quercetin attenuated inflammatory responses and HO in vivo. Furthermore, elevated SIRT1 and decreased acetylated NFκB p65 expression were responsible for the mechanism of quercetin, and the beneficial effects of quercetin were reversed by the SIRT1 antagonist EX527 and mimicked by the SIRT agonist SRT1720. The findings in this study suggest that targeting monocyte/macrophage and mast cell activities may represent an attractive approach for therapeutic intervention of HO and that quercetin may serve as a promising therapeutic candidate for the treatment of trauma-induced HO by modulating SIRT1/NFκB signaling.

Quercetin Alleviates Oxidative Damage by Activating Nuclear Factor Erythroid 2-Related Factor 2 Signaling in Porcine Enterocytes.

Oxidative stress has been implicated in the etiology of multiple gastrointestinal disorders, such as irritable bowel syndrome and inflammatory bowel disease. This study was conducted to evaluate effects of natural product quercetin on diquat-induced oxidative stress in porcine enterocytes and underlying mechanisms. Intestinal porcine epithelial cell line 1 (IPEC-1) cells pretreated with or without quercetin (5 μM, 24 h) were incubated with vehicle or diquat (100 μM) for 6 h. The results showed that diquat treatment induced apoptosis in a caspase-3-dependent manner, as accompanied by elevated reactive oxygen species (ROS) production, increased mitochondrial depolarization, and reduced the abundance of tight junction proteins. These adverse effects of diquat were remarkably abrogated by quercetin administration. Further study indicated that the protective effect of quercetin was associated with elevated protein abundance of nuclear factor erythroid 2-related factor 2 (Nrf2) and increased intracellular glutathione (GSH) content. Interestingly, the beneficial effects of quercetin on diquat-induced oxidative damage were abolished by all-trans-retinoic acid (Atra), a specific inhibitor of Nrf2, indicating a Nrf2-dependent regulation manner. The results show that quercetin attenuates diquat-induced cell injury by promoting protein abundance of Nrf2 and regulating GSH-related redox homeostasis in enterocytes. These findings provide new insights into a function role of quercetin in maintaining intestinal homeostasis.

New perspectives of quercetin and vitamin C effects on fibronectin-binding integrins and chemokine receptors in prostate cancer cell lines.

The aim of this study is to investigate the effect of two abundant dietary supplements, quercetin and vitamin C on some factors involved in metastasis and proliferation of prostate cancer, which are resistant to conventional chemotherapies in late stages. Bone and brain are two common sites of metastases in prostate cancer, nevertheless the factors involved in their metastatic pathways are not well understood. The effect of quercetin (75µM) and vitamin C (100 µM) on CXCR4, CXCR7 chemokine receptors, α4, α5 and β1 integrins, ki-67 proliferation marker and Vascular endothelial growth factor, VEGF was evaluated using Quantitative Reverse Transcription PCR (RT-qPCR). The effect of quercetin and vitamin C alone was different on PC3 and DU145 prostate cancer cell lines, but sequential combination reduced significantly the expression of CXCR and CXCR7 chemokine receptors, α4, α5 and β1 integrin subunits, VEGF and Ki-67 proliferation markers in PC3 and DU145 cell lines. Our results indicated the beneficial effect of quercetin and vitamin C on prostate cancer cells with different metastatic sites and their differential response to the treatment which in turn may lead us to reach suitable therapeutic outcomes to combat cancer (Fig. 3, Ref. 36).

Quercetin Combined With Human Umbilical Cord Mesenchymal Stem Cells Regulated Tumour Necrosis Factor-α/Interferon-γ-Stimulated Peripheral Blood Mononuclear Cells via Activation of Toll-Like Receptor 3 Signalling.

The beneficial effect of quercetin in rheumatic diseases is unclear. Studies have already confirmed that human umbilical cord mesenchymal stem cells (hUCMSCs) alleviate some symptoms of rheumatoid arthritis (RA) by their immunosuppressive capacities. This study explored whether there are additive effects of quercetin and hUCMSCs on peripheral blood mononuclear cells (PBMCs) under simulated rheumatic conditions. hUCMSCs were pretreated with quercetin (10 μM) before coculture with TNF-α/IFN-γ-stimulated PBMCs at a ratio of 1:1 for 3 days. PBMC proliferation was inhibited, and the proportion of Th17 cells was shifted. These effects may be related to the effect of quercetin on functional molecules in hUCMSCs, including nitric oxide (NO), indoleamine 2,3-dioxygenase (IDO), interleukin 6 (IL-6) and Toll-like receptor-3 (TLR-3) and the Akt/IκB pathways. These results suggest that quercetin effectively promoted the immunoregulatory effect of hUCMSCs by inhibiting the Akt/IκB pathway, activating the Toll-like receptor-3 pathway, and regulating downstream cytokines.

Beneficial Effect of Quercetin Against Dimethoate Induced Cerebellar Cortex Injury in Adult Male Albino Rat: Histological and Immunohistochemical Study

Abstract Background: The organophosphorus compound dimethoate is pesticide that widely used across the world to control worms and insects. It is highly toxic and causes neurobehavioral disorders. Quercetin is a natural flavonoid that is profusely found in fruits and vegetablesand is known for its antioxidants property and its ability to improve oxidative stress and promote cellular survival. Aim of Study: To assess neurotoxicity and structural alterations of cerebellar cortex caused by dimethoate and explore the neuroprotective potential effect of quercetin. Material and Methods: The study was carried out on 32 adult, male Wister albino rats weighing 180-200g, they were randomly divided into four groups: Normal control, dimethoate treated (30mg/kg alternate day), quercetin treated (50mg/kg daily) and combined dimethoate + quercetin treated. All the treatments continued for 60 days. All animals were anesthe-tized, cerebellum was removed to prepare the specimens for histological, immunohistochemical and biochemical exami-nation. Results: The results revealed asign of toxicity and a significant decrease in body weight of animals treated with dimethoate which were substantially improved upon concurrent supplementation with quercetin. Further, treatment with dimethoate resulted in a significant decrease in the activity of acetyl cholinesterase in cerebellum tissue which was increased upon co-treatment with quercetin. On the contrary, we noticed a significant increase in the levels of MDA in cerebellum which were revealed significant reduction upon supplementation of quercetin. Light microscopic examination of cerebellum showed histoarchitectural alterations with significant up regulation of apoptotic marker (caspase-3) and astrogliosis marker Glial Fibrillary Acidic Protein (GFAP) in cerebellar tissue, Although, there were a significant down regulation of synaptophysin (SYP) immunoexpression. These changes were improved upon co-treatment with quercetin. Therefore, we conclude that quercetin when used as a prophy-lactic intervention would afford safeguard against dimethoate induced neurotoxicity.

The effects of quercetin on antioxidant and cytokine levels in rat hippocampus exposed to acute cadmium toxicity

 The aim of this study was to determine cadmium neurotoxicity (Branca et al.  2018) and beneficial effect of quercetin (QE) (Kanter et al.  2016) against on neuronal damage in hippocampus exposed with acute cadmium (Cd). Adult male Wistar-Albino rats (n = 30) were used and divided into four groups as Control (C, n = 6), Cadmium (Cd, n = 8), Quercetin (Q, n = 8) and Cadmium + Quercetin (Cd + Q, n = 8). Cadmium (CdCl2, 4 mg kg-1 daily, s.c) were administrated to Cd and Cd+Q groups, and Quercetin (Q, 50 mg kg-1 daily, i.p) were administrated to Q and Cd + Q groups for 3 days, respectively. At 4th day after the treatments, hippocampal samples were taken from the four groups. Cadmium decreased superoxide dismutase (SOD) and reduced glutathione (GSH) levels and the SOD activity and GSH level were markedly (p< 0.05) lower in Cd group than in the Q and C groups. Lipid peroxidation (MDA) levels were higher in Cd group when compared to the control, Q and Cd+Q groups. IL1 levels were found statistically higher in Cd group than in the control, Q and Cd+Q groups. IL-6 and TNF-alfa levels were significantly (p< 0.05) higher in Cd and Cd+Q groups than the Q and C groups.  In addition, IL10 levels were detected the lowest in Cd group when compared to other groups.      In conclusion, our results show that quercetin can be beneficial against to neurotoxic effects of acute cadmium toxicity in the rat hippocampus through upregulation of antioxidant system but down regulation of cytokine levels. 

Ameliorative role of quercetin in iron overload induced heart and brain toxicity in adult male albino rats

Although iron is an essential element for life, its excess is linked to many disorders. The aim of this study is to investigate the effect of quercetin on iron induced toxicity on the heart and brain in adult male albino rats. 50 adult male albino rats were equally divided into groups; Group I (negative control), Group II (positive control) received normal saline 0.9%. Group III (Quercetin group) was treated with quercetin (2 g/kg daily) for 8 weeks and Group IV (Iron group) was injected intraperitoneal daily with iron dextran (300 mg/kg) for 4 weeks. Group V (Iron and quercetin group) was injected intraperitoneal daily with iron dextran (300 mg/kg) for 4 weeks, and then gavaged orally with quercetin (2 g/kg once a day) for another 4 weeks. At the end of the study, blood samples were taken to estimate the serum levels of iron, malondialdehyde (MDA), and total antioxidant capacity (TAC). Heart and brain specimens were dissected from scarified rats to estimate tissue level of iron, histopathological examination, immunohistochemical staining for tumor necrosis factor (TNFα) and comet assay. Iron overload caused increases in serum, heart and brain iron levels; increase in serum MDA and decrease in serum TAC with degenerative changes in the examined tissues and increasing expression of TNFα and DNA degradation. After administration of quercetin, a significant improvement in all these parameters was observed. Quercetin acts as iron chelator decreasing serum and tissue iron levels, ameliorating oxidative stress, inflammatory effects and DNA damage induced by iron overload. More studies are recommended to evaluate the beneficial effects of quercetin with iron excess. Key words: Iron, quercetin, heart toxicity, brain toxicity.

Mitochondrial Electron Transport Chain Complex Dysfunction in MeCP2 Knock-Down Astrocytes: Protective Effects of Quercetin Hydrate.

Astrocytes play the central role in CNS metabolism to support neuronal functions. Mehyl-CpG-binding protein 2 (MeCP2) is the global transcription factor with differential expression in neuronal and non-neuronal cells. MeCP2 mutation and downstream detrimental effects have been reported in astrocytes also in MeCP2-associated neurodevelopmental disorder-Rett syndrome. Several studies have shown mitochondrial impairment linked to ROS production and reduced ATP synthesis in Rett patients and models, but consequences of MeCP2 deficiency on mitochondrial electron transport chain complexes in astrocytes and effect of known antioxidant quercetin aglycone has not yet been reported. The present study aimed to investigate effect of quercetin on mitochondrial functioning in MeCP2-deficient astrocytes. Our data show onefold upregulated Uqcrc1 and Ndufv2 gene expression, subtle change in protein expression, and significantly reduced mitochondrial respiratory chain complex-II and complex-III enzyme activities in MeCP2 knock-down astrocytes. Intracellular calcium robustly increased and mitochondrial membrane potential decreased, while no change in ROS was observed in MeCP2 knock-down astrocytes. Quercetin increased MeCP2 and normalized Uqcrc1 and Ndufv2 gene expression but did not modulate MeCP2 and Ndufv2 proteins expression. Interestingly, quercetin upregulated significantly the mitochondrial respiratory complex-II, complex-III, and complex-IV activities in dose-dependent manner. It also restored intracellular calcium level and mitochondrial membrane potential. In vitro observations suggest the beneficial effect of quercetin in mitochondrial functioning in MeCP2-deficient condition. There are no reports focusing on role of quercetin in mitochondrial function in MeCP2-deficient astrocytes, and these observations serve as preliminary data to evaluate quercetin's effects in vivo.

Beneficial Effects of Quercetin on the Zone of Stasis in an Experimental Burn Model

Beneficial Effects of Quercetin on the Zone of Stasis in an Experimental Burn Model

Querectin improves myelin repair of optic chiasm in lyolecithin-induced focal demyelination model

Although the beneficial effects of quercetin on oligodendrocyte precursor cell (OPCs) population has been evaluated in-vitro, there are few studies about the effects of quercetin on myelin repair in the context of demyelination. The aim of this study was to investigate the effects of querectin on functional recovery and myelin repair of optic chiasm in lysolecithin (LPC)-induced demyelination model. Demyelination was induced by local injection of LPC 1% (2 μl) into rat optic chiasm. Querectin at doses 25 or 50 mg/kg was administrated daily by oral gavage for 7 or 14 days post LPC. Visual evoked potential (VEPs) recordings were used to assess the functional property of the optic pathway. Immunostaining and myelin staining were performed on brain sections 7 or 14 days post lesion. Electrophysiological data indicated that LPC injection increased the latency of VEPs waves and quercetin effectively reduced the delay of visual signals. The level of glial activation was alleviated in animals under treatment of quercetin compared to vehicle group. Furthermore, quercetin treatment decreased the extent of demyelination areas and increased the remyelination process following LPC injection. Overall, our findings indicate that quercetin could remarkably improve the functional recovery of the optic pathway by its protective effects on myelin sheath and attenuation of glial activation.

The Beneficial Effects of Quercetin, Curcumin, and Resveratrol in Obesity.

Over the past two decades, obesity has been one of the major public health concerns in most countries. In the search for new molecules that could be used for the treatment of obesity, good perspectives have been opened up for polyphenols, a class of natural bioactive phytochemicals. Experimental and limited clinical trial evidence supports that some polyphenols such as quercetin, curcumin, and resveratrol have potential benefit functions on obesity treatment. This brief review focuses on the main functions of the above-named polyphenols on adipose tissue. These polyphenols may play beneficial effects on adipose tissue under obese condition by alleviating intracellular oxidative stress, reducing chronic low-grade inflammation, inhibiting adipogenesis and lipogenesis, and suppressing the differentiation of preadipocytes to mature adipocytes.

Beneficial effects of quercetin on titanium dioxide nanoparticles induced spermatogenesis defects in mice.

Many recent studies have demonstrated that most nanoparticles (NPs) have an adverse or toxic action on male germ cells. In present study, protective effect of quercetin (Que) on titanium dioxide nanoparticle (NTiO2)-induced spermatogenesis defects in mice was investigated. Thirty-two Naval Medical Research Institute (NMRI) mice were randomly divided into four groups. Que group received 75mg/kg of Que for 42days. NTiO2 group received 300mg/kg NTiO2 for 35days. NTiO2 + Que group initially received 75mg/kg Que for 7days and was followed by concomitant administration of 300mg/kg NTiO2 for 35days. Control group received only normal saline for 42days. Sperm parameters, testosterone concentration, histological criteria, and apoptotic index were assessed. Product of lipid peroxidation (MDA), superoxide dismutase (SOD), and catalase (CAT) activities were also evaluated for oxidative stress in testicular tissue. Administration of NTiO2 significantly induced histological changes in testicular tissue; increased apoptotic index; and decreased testicular weight, testosterone concentration, and sperm quality (p<0.01). In the testis, NTiO2 increased oxidative stress through an increase in lipid peroxidation and a decrease in SOD and CAT activities (p<0.05). Que pretreatment could significantly attenuate testicular weight; apoptotic index; and histological criteria including vacuolization, detachment, and sloughing of germ cells in seminiferous tubules. Serum and tissue testosterone levels were significantly increased in Que-pretreated mice (p<0.01). Sperm parameters including sperm number, motility, and percentage of abnormality were also effectively improved by Que pretreatment (p<0.01). Pretreatment of Que significantly ameliorated oxidative stress and increased the activities of SOD and CAT in testicular tissue. These results indicate that sperm production can be increased by Que pretreatment in NTiO2-intoxicated mice. The improved sperm quality and reverse testis histology by Que pretreatment may be a consequence of elevation testosterone concentration, reduction in germ cell apoptosis, and suppression of oxidative stress in testicular tissue.