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1.
Article in Chinese | WPRIM | ID: wpr-879018

ABSTRACT

Chemical constituents were isolated and purified from the water extract of Artemisia annua by column chromatography of HP-20 macroporous resin, silica gel, ODS, Sephadex LH-20, HW-40, and semi-preparative RP-HPLC. Their structures were elucidated by physicochemical properties and spectral analyses. As a result, Fifteen compounds were isolated and identified as vitexnegheteroin M(1), sibricose A5(2), securoside A(3), citrusin D(4), annphenone(5), E-melilotoside(6), esculetin(7), scopoletin-7-O-β-D-glucoside(8), eleutheroside B_1(9), chrysosplenol D(10), patuletin-3-O-β-D-glucopyranoside(11), quercetin-7-O-β-D-glucoside(12), rutin(13), apigenin 6,8-di-C-β-D-glucopyranoside(14), isoschaftoside(15), among them, compounds 1-4 were identified from Artemisia for the first time. Additionally, the isolates were evaluated for their inhibitory effects on the production of PGE_2 in LPS-simulated RAW264.7 macrophages. The results showed that compounds 1, 2, 8, and 10-15 could reduce PGE_2 levels, to a certain extent.


Subject(s)
Apigenin , Artemisia annua , Quercetin , Rutin
2.
Int. j. morphol ; 38(4): 876-881, Aug. 2020. graf
Article in English | LILACS | ID: biblio-1124869

ABSTRACT

Acetaminophen (also called paracetamol, or APAP) causes acute kidney injury after accidental or intentional ingestion of a toxic dose of the drug. We tested whether the antioxidant and anti-inflammatory agent, quercetin (QUR) given alone can protect against acute nephrotoxicity induced by APAP overdose in a rat model of APAP-induced acute kidney injury. Rats were either given a single dose of APAP (2 g/kg) before being sacrificed after 24 hours or were pre-treated for 7 days with QUR (50 mg/kg) before being given a single dose of APAP and then sacrificed 24 hours post APAP ingestion. Kidneys were examined by light microscopy after staining with hematoxylin and eosin (H&E) and collected blood samples were assayed for biomarkers of oxidative stress, inflammation, and kidney injury. H&E stained sections of kidney from the model group of rats (APAP) showed substantial damage to the kidney architecture as demonstrated by widening of Bowman's space, tubular dilatation, vacuolization of tubular epithelium, and congested dilated blood vessels, which were partially protected by QUR. In addition, APAP significantly (p<0.05) increased blood levels of urea, creatinine, malondialdehyde (MDA), tumor necrosis factor-alpha (TNF-a), and interleukin-6 (IL-6), which were significantly (p<0.05) reduced by QUR. These results indicate that quercetin partially protects against APAP-induced acute kidney injury in rats, which is associated with the inhibition of biomarkers of oxidative stress and inflammation and kidney injury.


El acetaminofeno (también llamado paracetamol o DCI) causa daño renal agudo después de la ingestión accidental o intencional de una dosis tóxica del medicamento. En el estudio analizamos si el agente antioxidante y antiinflamatorio, la quercetina (QUR) administrada sola, puede proteger contra la nefrotoxicidad aguda inducida por sobredosis de DCI en un modelo de rata. Las ratas recibieron una dosis única de DCI (2 g / kg) antes de ser sacrificadas después de 24 horas o fueron pretratadas durante 7 días con QUR (50 mg / kg) antes de recibir una dosis única de DCI y luego sacrificadas 24 horas post ingestión. Los riñones se examinaron mediante microscopía óptica después de la tinción con hematoxilina y eosina (H&E) y las muestras de sangre recolectadas se analizaron para detectar biomarcadores de estrés oxidativo, inflamación y daño renal. Las secciones de riñón teñidas con H&E del grupo modelo de ratas (DCI) mostraron un daño sustancial a la arquitectura del riñón, como lo demuestra la ampliación del espacio de Bowman, la dilatación tubular, la vacuolización del epitelio tubular y los vasos sanguíneos dilatados congestionados, que estaban parcialmente protegidos por QUR. Además, DCI aumentó significativamente (p <0,05) los niveles sanguíneos de la urea, creatinina, malondialdehído (MDA), factor de necrosis tumoral alfa (TNF-a) e interleucina-6 (IL-6), los que fueron reducidos significativamente (p < 0,05) por QUR. Estos resultados indican que la quercetina protege parcialmente contra la lesión renal aguda inducida por DCI en ratas, asociada con la inhibición de biomarcadores de estrés oxidativo, inflamación y lesión renal.


Subject(s)
Animals , Rats , Quercetin/administration & dosage , Acute Kidney Injury/chemically induced , Acetaminophen/toxicity , Antioxidants/administration & dosage , Quercetin/pharmacology , Biomarkers/analysis , Oxidative Stress/drug effects , Protective Agents , Creatinine , Disease Models, Animal , Inflammation , Kidney/drug effects , Antioxidants/pharmacology
3.
Int. j. morphol ; 38(3): 585-591, June 2020. graf
Article in English | LILACS | ID: biblio-1098291

ABSTRACT

Acetaminophen (also called paracetamol, or APAP) induced nephrotoxicity is reported after accidental or intentional ingestion of an overdose of the drug. Renal tubular ultrastructural alterations induced by APAP overdose associated with the induction of biomarkers of kidney injury have not been investigated before. Also, we investigated whether the combined polyphenolic anti-inflammatory and antioxidants agents, resveratrol (RES) and quercetin (QUR) can protect against APAP-induced acute kidney injury. The model group of rats received a single dose of APAP (2 g/kg), whereas the protective group of rats was pre-treated for 7 days with combined doses of RES (30 mg/kg) and QUR (50 mg/kg) before being given a single dose of APAP. All rats were then sacrificed one day post APAP ingestion. Harvested kidney tissues were prepared for transmission electron microscopy (TEM) staining and blood samples were assayed for urea, creatinine, and biomarkers of inflammation and oxidative stress. TEM images and blood chemistry analysis showed that APAP overdose induced kidney damage as demonstrated by substantial alterations to the proximal convoluted tubule ultrastructure, and a significant (p<0.05) increase in urea, creatinine, tumor necrosis factor-alpha (TNF-a), and malondialdehyde (MDA) blood levels, which were protected by RES+QUR. These findings indicate that APAP induces alterations to the renal tubular ultrastructure, which is inhibited by resveratrol plus quercetin, which also decreases blood levels of kidney injury biomarkers.


El objetivo de este trabajo fue estudiar la nefrotoxicidad inducida por acetaminofeno (también llamado paracetamol o APAP) después de la ingestión accidental o intencional de una sobredosis de la droga. Las alteraciones ultraestructurales tubulares renales inducidas por sobredosis de APAP asociadas con la inducción de biomarcadores de daño renal no se han investigado. Además, estudiamos si los agentes combinados antiinflamatorios y antioxidantes polifenólicos, el resveratrol (RES) y la quercetina (QUR) pueden proteger contra la lesión renal aguda inducida por APAP. El grupo modelo de ratas recibió una dosis única de APAP (2 g / kg), mientras que el grupo protector de ratas se trató previamente durante 7 días con dosis combinadas de RES (30 mg / kg) y QUR (50 mg / kg) antes de recibir una dosis única de APAP. Todas las ratas se sacrificaron un día después de la ingestión de APAP. Los tejidos renales fueron preparados para el análisis a través de la microscopía electrónica de transmisión (MET). En las muestras de sangre se determinaron la urea, creatinina y los biomarcadores de inflamación y estrés oxidativo. Las imágenes MET y el análisis químico de la sangre mostraron que la sobredosis de APAP inducía daño renal, como lo demuestran las alteraciones sustanciales en la ultraestructura del túbulo contorneado proximal, y además, de un aumento significativo (p <0,05) de la urea, creatinina, factor de necrosis tumoral alfa y niveles sanguíneos de malondialdehído, protegidos por RES + QUR. Estos hallazgos indican que APAP induce alteraciones en la ultraestructura tubular renal, inhibida por el resveratrol más quercetina, que también disminuye los niveles sanguíneos de biomarcadores de daño renal.


Subject(s)
Animals , Rats , Quercetin/administration & dosage , Resveratrol/administration & dosage , Kidney Tubules/drug effects , Acetaminophen/toxicity , Quercetin/pharmacology , Urea/blood , Rats, Sprague-Dawley , Creatinine/blood , Microscopy, Electron, Transmission , Disease Models, Animal , Drug Overdose , Resveratrol/pharmacology , Kidney Tubules/pathology , Anti-Inflammatory Agents/administration & dosage , Antioxidants/administration & dosage
4.
Int. j. morphol ; 38(1): 83-90, Feb. 2020. tab, graf
Article in English | LILACS | ID: biblio-1056402

ABSTRACT

We sought to determine whether the combined polyphenolic compounds, resveratrol and quercetin can substantially protect against modulation of hepatic biomarkers of apoptosis and survival, p53-Bax axis and B-cell lymphoma 2 (Bcl-2) in an animal model of acetaminophen-induced acute liver injury via the association of oxidative stress and interleukin-11 (IL-11). The model group of rats received a single dose of acetaminophen (2 g/kg), whereas the protective group of rats was pre-treated for 7 days with combined doses of resveratrol (30 mg/kg) and quercetin (50 mg/kg) before being given a single dose of acetaminophen. All rats were then sacrificed 24 hours post acetaminophen ingestion. Acetaminophen overdose induced acute liver injury as demonstrated by profound liver parenchymal damage and increased levels of the liver injury enzymes, alanine aminotransferase (ALT) and aspartate aminotransferase (AST). Acetaminophen significantly (p<0.05) modulated malondialdehyde (MDA), p53, apoptosis regulator Bax, Bcl-2, IL-11, interleukin-6 (IL-6), ALT, AST, superoxide dismutase (SOD), and glutathione peroxidase (GPx), which were significantly protected by resveratrol plus quercetin. We further demonstrated a significant (p<0.01) correlation between IL-11 scoring and the levels of p53, Bax, Bcl-2, and MDA. Thus, resveratrol plus quercetin effectively protect against acetaminophen-induced apoptosis, which is associated with the inhibition of oxidative stress and IL-11.


En el estudio se intentó determinar si los compuestos polifenólicos combinados, el resveratrol y la quercetina pueden proteger sustancialmente contra la modulación de los biomarcadores hepáticos de apoptosis y supervivencia, el eje p53-Bax y el linfoma de células B 2 (Bcl-2) en un modelo animal de lesión hepática aguda inducida por acetaminofén, a través de la asociación del estrés oxidativo y la interleucina-11 (IL-11). El grupo modelo de ratas recibió una dosis única de acetaminofén (2 g / kg), mientras que el grupo protector de ratas fue tratado durante 7 días con dosis combinadas de resveratrol (30 mg / kg) y quercetina (50 mg / kg) antes de recibir una dosis única de acetaminofén. Todas los animales fueron sacrificados 24 horas después de la ingestión de acetaminofén. La sobredosis de acetaminofén indujo una lesión hepática aguda, como se observó en el daño profundo del parénquima hepático y el aumento de los niveles de las enzimas en la lesión hepática, alanina aminotransferasa (ALT) y aspartato aminotransferasa (AST). Acetaminofén moduló significativamente (p <0.05) malondialdehído (MDA), p53, regulador de apoptosis Bax, Bcl2, IL-11, interleucina-6 (IL-6), ALT, AST, superóxido dismutasa (SOD) y glutatión peroxidasa ( GPx), los que se encontraron significativamente protegidos por el resveratrol y quercetina. Además se determinó una correlación significativa (p <0.01) entre la puntuación de IL-11 y los niveles de p53, Bax, Bcl-2 y MDA. En conclusión, el resveratrol más la quercetina protegen de manera efectiva contra la apoptosis inducida por acetaminofén, asociada con la inhibición del estrés oxidativo y la IL-11.


Subject(s)
Animals , Rats , Quercetin/administration & dosage , Apoptosis/drug effects , Chemical and Drug Induced Liver Injury, Chronic/pathology , Resveratrol/administration & dosage , Acetaminophen/toxicity , Antioxidants/administration & dosage , Quercetin/pharmacology , Aspartate Aminotransferases/analysis , Biomarkers , Interleukin-1 , Oxidative Stress , Alanine Transaminase/analysis , Disease Models, Animal , Chemical and Drug Induced Liver Injury/enzymology , Resveratrol/pharmacology , Antioxidants/pharmacology
6.
Article in English | WPRIM | ID: wpr-881038

ABSTRACT

Due to the poor repair ability of cartilage tissue, regenerative medicine still faces great challenges in the repair of large articular cartilage defects. Quercetin is widely applied as a traditional Chinese medicine in tissue regeneration including liver, bone and skin tissues. However, the evidence for its effects and internal mechanisms for cartilage regeneration are limited. In the present study, the effects of quercetin on chondrocyte function were systematically evaluated by CCK8 assay, PCR assay, cartilaginous matrix staining assays, immunofluorescence assay, and western blotting. The results showed that quercetin significantly up-regulated the expression of chondrogenesis genes and stimulated the secretion of GAG (glycosaminoglycan) through activating the ERK, P38 and AKT signalling pathways in a dose-dependent manner. Furthermore, in vivo experiments revealed that quercetin-loaded silk protein scaffolds dramatically stimulated the formation of new cartilage-like tissue with higher histological scores in rat femoral cartilage defects. These data suggest that quercetin can effectively stimulate chondrogenesis in vitro and in vivo, demonstrating the potential application of quercetin in the regeneration of cartilage defects.


Subject(s)
Animals , Cartilage/cytology , Chondrocytes/drug effects , Chondrogenesis/drug effects , Extracellular Matrix/metabolism , Quercetin/pharmacology , Rats , Signal Transduction/drug effects , Tissue Scaffolds
7.
Chinese Journal of Biotechnology ; (12): 2877-2891, 2020.
Article in Chinese | WPRIM | ID: wpr-878537

ABSTRACT

Studies on the interaction between small organic molecules and DNA are important means to explore drug mechanism and new drugs. Quercetin is a polyhydroxy flavone compound with activities such as anti-cancer, anti-inflammatory, antibacterial, antiviral, hypoglycemic and anti-hypertensive, immunomodulation and cardiovascular protection. Experimental studies aim at confirming if an interaction exists between quercetin and DNA, and determining the type of interaction. The interaction between quercetin and herring DNA can be detected by fluorescence spectrometry and resonance scattering fluorescence spectrometry analysis. The mode of the interaction between quercetin and herring DNA can be detected by UV-Vis spectrophotometry and fluorescence polarization analysis. This review helps understand the in vitro interaction between quercetin and DNA, and assist the development of drugs for corresponding diseases.


Subject(s)
DNA/genetics , Quercetin , Spectrometry, Fluorescence
8.
Chinese Journal of Biotechnology ; (12): 2838-2849, 2020.
Article in Chinese | WPRIM | ID: wpr-878533

ABSTRACT

(2S)-taxifolin is an important flavonoid that has anti-inflammatory and anti-oxidation effects. It is widely used in pharmaceutical and nutraceutical industries. Flavone 3-hydroxylase (F3H) can catalyze the synthesis of (2S)-taxifolin and other 3-hydroxylated flavonoids from (2S)-eriodictyol. Due to the low catalytic efficiency of F3H, the titer of many 3-hydroxyflavones, such as taxifolin, synthesized by microbial method is relatively low. In this study, a SmF3H was identified from the transcriptome of Silybum marianum (L.) Gaertn. The results of fermentation showed that SmF3H can catalyze the flavone 3-hydroxylation reaction, and its catalytic efficiency was significantly higher than that of commonly used SlF3H from Solanum lycopersicum. Six promoters with different transcription strength were selected to optimize the synthesis pathway from the flavonoid precursor (2S)-naringenin to (2S)-taxifolin. The results showed that the highest titer of (2S)-taxifolin (695.90 mg/L in shake flask) could be obtained when the P(GAL7) promoter was used to control the expression of SmF3H. The titer of (2S)-taxifolin was further improved to 3.54 g/L in a 5-L fermenter, which is the highest titer according to current available literatures.


Subject(s)
Antioxidants , Flavonoids , Milk Thistle , Quercetin/analogs & derivatives
9.
Article in Chinese | WPRIM | ID: wpr-828411

ABSTRACT

Quercetin is a kind of typical flavonoid, mainly found in various vegetables, fruits and Chinese herbs that are consumed daily, with the functions of anti-oxidation, anti-tumor, prevention and treatment of cardiovascular and cerebrovascular diseases. Quercetin is a natural compound with defined anti-tumor activity. Due to its low bioavailability and poor water solubility, quercetin has limitations in clinical application. The quercetin derivatives with good solubility, high bioavailability, metabolic stability, and low toxicity have been obtained through modification of quercetin structure. In recent years, a large number of quercetin ethers, esters, complexes, C-4 carbonyloxy substituted derivatives, A,B-ring modified compounds and other derivatives have been synthesized and tested for in vitro anticancer activity. The quercetin derivatives with anti-tumor activity synthesized in the last 5 years were reviewed in this paper.


Subject(s)
Biological Availability , Humans , Neoplasms , Oxidation-Reduction , Quercetin , Solubility
10.
Article in Chinese | WPRIM | ID: wpr-828410

ABSTRACT

Myricetin and its glycosides are important flavonols commonly found in plants, and they are natural organic compounds with diverse pharmacological activities. Numerous studies have demonstrated that myricetin and its glycosides are strong antioxidants that have great potential in preventing, alleviating and assisting the treatment of chronic non-infectious diseases such as cancer, diabetes, and cardiovascular diseases. In addition, myricetin and its glycosides also have antiviral, antibacterial, anti-inflammatory, analgesic, liver protection and other pharmacological activities. Myricetin contains more hydroxyl groups in the parent ring structure than other flavonoids, so myricetin and its glycosides have stronger pharmacological activities than other flavonols or flavonoids such as quercetin and kaempferol. Therefore, myricetin and its glycosides have great development and application prospects. In this paper, the classification and distribution of myricetin and its glycosides, their pharmacological activity and mechanism, as well as comparison with other flavonoids were reviewed. In addition, limitations of the current research and application of myricetin and its glycosides were analyzed, and the further studies on pharmacological activities as well as their dose-activity relationship, structure-activity relationship, chemical modification, biosynthesis and application prospects of myricetin and its glycosides were discussed and proposed.


Subject(s)
Flavonoids , Flavonols , Glycosides , Quercetin
11.
Journal of Experimental Hematology ; (6): 1234-1239, 2020.
Article in Chinese | WPRIM | ID: wpr-827134

ABSTRACT

OBJECTIVE@#To investigate the effect of quercetin (que) on proliferation and apoptosis of multiple myeloma cell line NCI-H929.@*METHODS@#NCI-H929 cells were routinely cultured, and cells in logarithmic growth phase were taken and used for experiments. After treatment of NCI-H929 cells with Que of 50, 100 and 200 µmol/ L for 24, 48 and 72 hours, the proliferation level of cells was detected by using MTT method; after treatment of NCI-H929 cells with Que of 100 and 200 µmol/ L for 24 hours, the cell apoptosis level was detected by Annexin V-FITC/PI double staining, the changes of cell cycle was analysis by flow cytometry with PI marking; the expression of apoptosis-related proteins caspase-3, caspase-8, caspase-9, PARP, BCL-2 and cell cycle-related proteins P53, P21, P27, CDK4, and the activiation of ERK and ATK were detected by Western blot.@*RESULTS@#Que of different concentration could inhibit cell proliferation with time and dose dependent manner. The flow cytometry showed that Que could significantly increase the cell apoptosis and arrest NCI-H929 cells in the G/M phase. In addition, Western blot analysis showed that Que could activate the apoptosis-related proteins, such as caspase-3, caspase-8, caspase-9 and PARP, and then inhibited the expression of BCL-2. Que could promote the expression of P53, P21 and P27, however, it could inhibited the CDK4 expression in NCI-H929 cells. Que could decrease the phosphorylation levels of p-ERK and p-AKT in NCI-H929 cells.@*CONCLUSION@#Quercetin mediates anti-myeloma effects through inducing apoptosis, cell cycle arrest and down-regulating ERK and AKT pathways in human myeloma cells.


Subject(s)
Apoptosis , Cell Line, Tumor , Cell Proliferation , Humans , Multiple Myeloma , Quercetin
12.
Article in English | WPRIM | ID: wpr-787137

ABSTRACT

Aging is one of the risk factors for the development of cardiovascular diseases. During the progression of cellular senescence, cells enter a state of irreversible growth arrest and display resistance to apoptosis. As a flavonoid, quercetin induces apoptosis in various cells. Accordingly, we investigated the relationship between quercetin-induced apoptosis and the inhibition of cellular senescence, and determined the mechanism of oxidative stress-induced vascular smooth muscle cell (VSMC) senescence. In cultured VSMCs, hydrogen peroxide (H₂O₂) dose-dependently induced senescence, which was associated with increased numbers of senescence-associated β-galactosidase-positive cells, decreased expression of SMP30, and activation of p53-p21 and p16 pathways. Along with senescence, expression of the anti-apoptotic protein Bcl-2 was observed to increase and the levels of proteins related to the apoptosis pathway were observed to decrease. Quercetin induced apoptosis through the activation of AMP-activated protein kinase. This action led to the alleviation of oxidative stress-induced VSMC senescence. Furthermore, the inhibition of AMPK activation with compound C and siRNA inhibited apoptosis and aggravated VSMC senescence by reversing p53-p21 and p16 pathways. These results suggest that senescent VSMCs are resistant to apoptosis and quercetin-induced apoptosis attenuated the oxidative stress-induced senescence through activation of AMPK. Therefore, induction of apoptosis by polyphenols such as quercetin may be worthy of attention for its anti-aging effects.


Subject(s)
Aging , AMP-Activated Protein Kinases , Apoptosis , Cardiovascular Diseases , Cellular Senescence , Hydrogen Peroxide , Muscle, Smooth, Vascular , Polyphenols , Quercetin , Risk Factors , RNA, Small Interfering
13.
Int. j. morphol ; 37(4): 1422-1428, Dec. 2019. graf
Article in English | LILACS | ID: biblio-1040148

ABSTRACT

Paracetamol (also called acetaminophen, or APAP) overdose causes acute damage to the liver and kidneys in both humans and experimental animal models via the induction of the oxidative stress pathway. We sought to determine whether the combined antioxidants and anti-inflammatory compounds, resveratrol (RES) and quercetin (QUR) can protect against kidney injury induced by a toxic dose of APAP in a rat model of APAP-induced acute kidney injury. Rats were either received a single dose of APAP (2 g/kg) before being sacrificed after 24 hours or were pre-treated for 7 days with combined doses of RES (30 mg/kg) and QUR (50 mg/kg) before being given a single dose of APAP and then sacrificed 24 hours post APAP ingestion. Harvested kidney tissues were prepared for light microscopy staining, and tissue samples were assayed for (i) biomarkers of oxidative stress and antioxidant, malondialdehyde (MDA) and superoxide dismutase (SOD); and (ii) biomarkers of inflammation, tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6). Hematoxylin and eosin (H&E) stained images showed that APAP overdose induced acute kidney injury as demonstrated by widening of glomeruli space (Bowman space), tubular dilatation, numerous cellular debris in the renal tubules with tubular epithelial degeneration, and vacuolization, which were effectively protected by RES+QUR except a partial protection of the glomeruli space was observed. In addition, APAP significantly (p<0.05) modulated tissue levels of MDA, SOD, TNF-α, and IL-6, which were protected by RES+QUR. Furthermore, a significant (p<0.0001) positive correlation was observed between glomeruli space and TNF-α, (r=0.8899), IL-6 (r=0.8986), and MDA (r=0.8552), whereas glomeruli space scoring versus SOD showed negative correlation (r= - 0.7870). We conclude that resveratrol plus quercetin substantially protects against APAP-induced acute kidney injury in rats, possibly via the augmentation of antioxidants and inhibition of oxidative stress and inflammation.


La sobredosis de paracetamol (también llamado acetaminofen o APAP) causa un daño agudo en el hígado y los riñones, tanto en humanos como en modelos animales experimentales, a través de la inducción de la vía del estrés oxidativo. Intentamos determinar si los antioxidantes y los compuestos antiinflamatorios combinados, el resveratrol (RES) y la quercetina (QUR) pueden proteger contra la lesión renal inducida por una dosis tóxica de APAP en un modelo de rata de lesión renal aguda inducida por APAP. Las ratas recibieron una dosis única de APAP (2 g / kg) antes de ser sacrificadas después de 24 horas o se trataron previamente durante 7 días con dosis combinadas de RES (30 mg / kg) y QUR (50 mg / kg), antes de ser tratadas, se administró una dosis única de APAP y luego fueron sacrificadas 24 horas después de la ingestión. Los tejidos renales recolectados se tiñeron con H-E y fueron observados a través de microscopía óptica. Las muestras de tejido se analizaron para (i) biomarcadores de estrés oxidativo y antioxidante, malondialdehído (MDA) y superóxido dismutasa (SOD); y (ii) biomarcadores de inflamación, factor de necrosis tumoral alfa (TNF-α) e interleucina-6 (IL-6). Las imágenes teñidas con H & E mostraron que la sobredosis de APAP indujo daño renal agudo como lo demuestra la ampliación del espacio glomerular, la dilatación tubular, numerosos desechos celulares en los túbulos renales con degeneración epitelial tubular y la vacuolización, que se protegieron eficazmente con RES + QUR Se observó una protección parcial del espacio glomerular. Además, APAP modificó significativamente (p <0.05) los niveles tisulares de MDA, SOD, TNF-α e IL-6, que estaban protegidos por RES + QUR. Además, se observó una correlación positiva significativa (p <0,0001) entre el espacio glomerular y el TNF-α, (r = 0,8899), IL-6 (r = 0,8986) y MDA (r = 0,8552), mientras que la puntuación del espacio glomerular versus SOD mostró correlación negativa (r = - 0,7870). Concluimos que el resveratrol más quercetina protege sustancialmente contra la lesión renal aguda inducida por APAP en ratas, posiblemente a través del aumento de antioxidantes y la inhibición del estrés oxidativo y la inflamación.


Subject(s)
Animals , Rats , Quercetin/therapeutic use , Acute Kidney Injury/drug therapy , Resveratrol/therapeutic use , Acetaminophen/toxicity , Quercetin/pharmacology , Oxidative Stress/drug effects , Disease Models, Animal , Drug Therapy, Combination , Acute Kidney Injury/chemically induced , Resveratrol/pharmacology , Acetaminophen/antagonists & inhibitors , Anti-Inflammatory Agents/therapeutic use , Antioxidants/therapeutic use
14.
Arq. gastroenterol ; 56(4): 405-411, Oct.-Dec. 2019. graf
Article in English | LILACS | ID: biblio-1055165

ABSTRACT

ABSTRACT BACKGROUND: Serotonin (5-HT) is present in the epithelial enterochromaffin cells (EC), mast cells of the lamina propria and enteric neurons. The 5-HT is involved in regulating motility, secretion, gut sensation, immune system and inflammation. OBJECTIVE: Evaluate the effects of diabetes and quercetin supplementation on serotoninergic cells and its cell loss by apoptosis in jejunal mucosa of streptozotocin-induced diabetic rats (STZ-rats). METHODS: Twenty-four male Wistar rats were divided into four groups: normoglycemic (C), normoglycemic supplemented with 40 mg/day quercetin (Q), diabetic (D) and diabetic supplemented with 40 mg/day quercetin (DQ). After 120 days, the jejunum was collected and fixated in Zamboni's solution for 18 h. After obtaining cryosections, immunohistochemistry was performed to label 5-HT and caspase-3. Quantification of 5-HT and caspase-3 immunoreactive (IR) cells in the lamina propria, villi and crypts were performed. RESULTS: The diabetic condition displayed an increase of the number of 5-HT-IR cells in villi and crypts, while decreased number of these cells was observed in lamina propria in the jejunum of STZ-rats. In the diabetic animals, an increased density of apoptotic cells in epithelial villi and crypts of the jejunum was observed, whereas a decreased number of caspase-3-IR cells was observed in lamina propria. Possibly, quercetin supplementation slightly suppressed the apoptosis phenomena in the epithelial villi and crypts of the STZ-rats, however the opposite effect was observed on the 5-HT-IR cells of the lamina propria. Quercetin supplementation on healthy animals promoted few changes of serotoninergic function and apoptotic stimuli. CONCLUSION: These results suggest that quercetin supplementation mostly improved the serotonergic function affected by diabetes maybe due to antioxidant and anti-inflammatory properties of quercetin.


RESUMO CONTEXTO: A serotonina (5-HT) está presente nas células epiteliais enterocromafins (CE), nos mastócitos da lâmina própria e nos neurônios entéricos. A 5-HT está envolvida na regulação da motilidade, secreção, nocepção intestinal, sistema imunológico e inflamação. Objetivo: Avaliar os efeitos do diabetes e da suplementação de quercetina sobre a função serotoninérgica e a perda celular por apoptose na mucosa jejunal de ratos diabéticos induzidos por estreptozotocina (ratos STZ). MÉTODOS: Vinte e quatro ratos Wistar machos foram divididos em quatro grupos: normoglicêmico (C), normoglicêmico suplementado com quercetina 40 mg/dia (Q), diabético (D) e diabético suplementado com quercetina 40 mg/dia (DQ). Após 120 dias, o jejuno foi coletado e fixado na solução de Zamboni por 18 horas. Após a obtenção de cortes em criostato, a imuno-histoquímica foi realizada para marcar 5-HT e caspase-3. A quantificação de células imunorreativas (IR) à 5-HT e caspase-3 foram realizadas na lâmina própria, vilosidades e criptas. RESULTADOS: A condição diabética ocasionou um aumento do número de células 5-HT-IR nas vilosidades e criptas, enquanto que na lâmina própria houve uma redução dessas células, no jejuno de ratos STZ. Nos animais diabéticos, foi observada uma densidade aumentada de células apoptóticas no epitélio do jejuno, tanto nas vilosidades quanto nas criptas, por outro lado um número reduzido de células caspase-3-IR foi observado na lâmina própria. Possivelmente, a suplementação de quercetina suprimiu ligeiramente os fenômenos de apoptose no epitélio de vilosidades e criptas do jejuno de ratos STZ, no entanto, o efeito oposto foi observado nas células 5-HT-IR da lâmina própria. A suplementação com quercetina em animais saudáveis promoveu poucas alterações na função serotoninérgica e nos estímulos apoptóticos. CONCLUSÃO: Estes resultados sugerem que a suplementação de quercetina melhorou principalmente a função serotoninérgica afetada pelo diabetes, talvez devido às propriedades antioxidantes e anti-inflamatórias da quercetina.


Subject(s)
Animals , Male , Rats , Quercetin/administration & dosage , Serotonin/metabolism , Apoptosis/drug effects , Dietary Supplements , Diabetes Mellitus, Experimental/drug therapy , Caspase 3/metabolism , Jejunum/pathology , Antioxidants/administration & dosage , Immunohistochemistry , Rats, Wistar , Diabetes Mellitus, Experimental/pathology , Interstitial Cells of Cajal/drug effects , Interstitial Cells of Cajal/pathology , Intestinal Mucosa/drug effects , Jejunum/drug effects
15.
Rev. bras. farmacogn ; 29(1): 69-76, Jan.-Feb. 2019. tab, graf
Article in English | LILACS | ID: biblio-990769

ABSTRACT

Abstract In this study, the adsorption/desorption characteristics of quercetin, luteolin and apigenin from Flos populi extract (Populus tomentosa Carrière, Salicaceae) on twelve macroporous resins (NKA-9, HPD-600, HPD-826, HPD-750, HPD-400, DM-130, AB-8, SP-825, X-5, D-101, HPD-100, HPD-200) were evaluated. Both high adsorption and desorption capacities of quercetin, luteolin and apigenin from Flos populi extract on SP-825 resin indicated that SP-825 resin was appropriate and its data were well fitted to the Langmuir and Freundlich isotherms. To get the optimal separation process, the influences of factors such as flow rates, loading sample volumes, concentrations of desorption solution were further investigated. Column packed with SP-825 resin was used to perform dynamic adsorption and desorption experiments. After one round of treatment, the contents of quercetin, luteolin and apigenin in the final products were 3.75-fold, 3.67-fold and 3.54-fold increased with recovery yields of 87.25, 85.19 and 82.22%, respectively. The results showed that the preparative enrichment of quercetin, luteolin and apigenin was available via adsorption and desorption on SP-825 resin. This method is a promising basis for the large-scale preparation of quercetin, luteolin and apigenin from Flos populi.


Subject(s)
Quercetin , Apigenin , Luteolin , Adsorption , Populus
16.
Article in Chinese | WPRIM | ID: wpr-772037

ABSTRACT

OBJECTIVE@#To investigate the protective effect of quercetin against lipopolysaccharide (LPS)- induced acute kidney injury (AKI) in mice and explore its mechanism.@*METHODS@#Forty male BALB/c mice were randomly divided into control group (with saline treatment), 15 mg/kg LPS group, and quercetin-treated groups with intragastric quercetin treatment (once daily for 3 consecutive days) at low (25 mg/kg) and high (50 mg/kg) dose prior to 15 mg/kg LPS injection. LPS was administered by intraperitoneally injection 1 after the last gavage of quercetin. The mice were sacrificed 24 h after LPS injection for analysis of kidney pathologies, blood urea nitrogen (BUN) and creatinine levels; serum levels of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and IL-6 were detected by ELISA, and the expressions of Toll-like receptor-4 (TLR4), MyD88, TRAF-6 and NF-κBp65 in the kidney were detected by Western blotting.@*RESULTS@#Quercetin significantly lessened renal pathologies, lowered BUN and creatinine levels ( < 0.05) and inhibited TNF-α, IL-1β, and IL-6 production in mice with LPS-induced AKI ( < 0.05). Pretreatment with quercetin also significantly inhibited TLR4, MyD88, and TRAF-6 expressions and NF-κBp65 activation in the kidneys of the rats with LPS challenge ( < 0.05).@*CONCLUSIONS@#Quercetin pretreatment can protect mice against LPSinduced AKI by inhibiting TLR4/NF-κB signaling pathway.


Subject(s)
Acute Kidney Injury , Animals , Antioxidants , Pharmacology , Lipopolysaccharides , Male , Mice , Mice, Inbred BALB C , NF-kappa B , Quercetin , Pharmacology , Rats , Toll-Like Receptor 4 , Tumor Necrosis Factor-alpha
17.
Article in Chinese | WPRIM | ID: wpr-773651

ABSTRACT

It is reported that energy metabolism is the core feature of tumor cells. This study is aimed to investigate the regulatory effect of two flavonoids( glabridin and quercetin) on energy supply and glycolysis of breast cancer cells,and provide reference for developing some anticancer herbal drugs with the function of regulating tumor energy metabolism. Based on the characteristics of each pathway during energy metabolism,in the present study,the triple negative breast cancer tumor cells( MDA-MB-231) were selected to investigate the effects of glabridin and quercetin on the energy metabolism of breast cancer cells and discuss the possible mechanisms from the following five potential targets: glucose uptake,protein expression of glucose transporter 1( GLUT1),adenosine triphosphate( ATP) level,lactate dehydrogenase( LDH) activity,and lactic acid( LD) concentration. The results showed that both quercetin and glabridin could decrease the glucose uptake capacity of breast cancer cells by down-regulating the protein expression of GLUT1. Quercetin had no significant effect on LDH activity and LD concentration; it did not affect the glycolysis process,but increased the intracellular ATP level. Glabridin decreased the activity of LDH and reduced LD concentration,thereby inhibiting the glycolysis metabolism of breast cancer cells. Therefore,both quercetin and glabridin can regulate the energy metabolism of breast cancer cells and can be used as potential anticancer agents or anti-cancer adjuvants.


Subject(s)
Breast Neoplasms , Metabolism , Cell Line, Tumor , Energy Metabolism , Glucose , Metabolism , Glucose Transporter Type 1 , Metabolism , Humans , Isoflavones , Pharmacology , Phenols , Pharmacology , Quercetin , Pharmacology
18.
Journal of Experimental Hematology ; (6): 1094-1103, 2019.
Article in Chinese | WPRIM | ID: wpr-775758

ABSTRACT

OBJECTIVE@#To investigate the chemotherapeutic efficency of quercetin sensitized adriamycin.@*METHOD@#CCK-8 was used to detect the inhibitory effect of different doses of adriamycin, quercetin and quercetin combined with adriamycin on the proliferation of primary leukemia cells from patients with clinically refractory acute leukemia. Quercetin, adriamycin and their combination were used to treat non-irradiated T-ALL leukemia mice to observe the changes of survival curve and myocardial injury.@*RESULT@#There was no significant difference in the inhibition rate of primary leukemia cell proliferation between the adriamycin concentration group (6, 0.6 and 0.06 μg/ml) and the adriamycin half-dose (3, 0.3 and 0.03 μg/ml) plus quercetin (0.25 mmol/L) group at three different time points (24, 48 and 72 hours). There was a significant difference in the inhibition rate of primary leukemia cell proliferation among the drug concentration groups, and the inhibition rate of primary leukemia cell proliferation was time-and concentration-dependent (r=0.995、r=1.000、r=0.984、r=0.993、r=0.999、r=0.960). In vivo experiments showed that the survival time of non-irradiated T-ALL leukemia mice treated with low-dose adriamycin combined with quercetin was not significantly prolonged compared with the high-dose adriamycin treatment group. The survival time of non-irradiated T-ALL leukemia mice treated with high dose of adriamycin and quercetin was significantly prolonged (P<0.05). Compared with adriamycin group, the SOD activity in adriamycin combined with quercetin group increased significantly and the MDA content decreased. The results of transcriptome sequencing analysis showed that the expression of Ighv1-84 and Igkv6-14 in adriamycin combined quercetin group and quercetin group was lower than that in adriamycin group. The Ms4a1, Podx1, Mecom, Sh3bgr12, Bex4 and Tdrp expression in adriamycin combined quercetin group and adriamycin group were higher than that in quercetin group, while Crabp1 expression was lower.@*CONCLUSION@#Quercetin can inhibit the proliferation of primary leukemia cells in a time-dependent manner. Quercetin combined with adriamycin inhibit the proliferation of primary leukemia cells significantly, and had synergistic and additive effects on the proliferation of primary leukemia cells, and the inhibiting effect of quercetin combined with adriamycin is concentration-and time-dependent. Quercetin combined with high-dose adriamycin can significantly prolong the survival time of non-irradiated T-ALL leukemia mice and reduce the myocardial damage caused by adriamycin.


Subject(s)
Animals , Apoptosis , Cell Proliferation , Doxorubicin , Humans , Leukemia, Myeloid, Acute , Mice , Quercetin
19.
Journal of Experimental Hematology ; (6): 1409-1415, 2019.
Article in Chinese | WPRIM | ID: wpr-775706

ABSTRACT

OBJECTIVE@#To investigate the effect of Quercetin (Qu) on cell proliferation, apoptosis and cell cycle, as well as the expression changes of Wnt/β-catenin signaling pathway, apoptosis and cell cycle regulators and BCR-ABL in CML susceptible cells K562 and imatinib-resistant cells (IM) K562R.@*METHODS@#The trypan blue staining was used to detect the all proliferation. The cell cycle and apoptosis were detected by flow cytometry. The fluorescence quantitative PCR and Western blot were used to detect the expression of mRNA and protein respectively.@*RESULTS@#After administration with 5, 10, 20, 40, 80, 160, 320 μmol/L Qu, the inhibition ratio in K562 cells was 5.07%, 5.98%, 11.09%, 31.88%, 56.89%, 70.44%, 86.63%; and that in K562R cells were 4.99%, 9.75%, 10.54%, 8.93%, 25.13%, 46.89%, 68.60%; IC of K562 and K562R was 76.4 μmol/L and 230.2 μmol/L, respectively. Flow cytometry showed that Qu (50, 100 and 200 μmol/L) could induce cell apoptosis and cell cycle arrest in a dose-dependent manner (r=0.9914, r=0.9871 respectively). After treatment with Qu (100 μmol/L),the expressions of mRNA (P<0.05) and protein(except Caspase-9) expression of Caspase-3, 8 and 9, p21 and p27 increased in K562 cells as compared with control, but the protein expression of p27 and Caspase-3 not changed in K562R. Qu (100 μmol/L) could decrease the mRNA(P<0.05) and protein levels of Wnt/β-catenin signaling pathway members GSK-3β, β-catenin, Lef-1 and the downstream targets PPAR-δ and Cyclin D1 compared with control. The PCR results showed that Qu could reduce the BCR-ABL mRNA expression in CML cells, but the protein expression of BCR-ABL and p-BCR-ABL not obviouly changed.@*CONCLUSION@#Qu can inhibit the proliferation K562 and K562R cells, and decrease the drug resistance and increase the sensitivity, that relate with inhibiting Wnt/β-catenin signaling pathway, activating apoptosis pathway and cyclins.


Subject(s)
Apoptosis , Cell Proliferation , Drug Resistance, Neoplasm , Glycogen Synthase Kinase 3 beta , Humans , K562 Cells , Leukemia, Myelogenous, Chronic, BCR-ABL Positive , Quercetin , Wnt Signaling Pathway , beta Catenin
20.
Journal of Experimental Hematology ; (6): 1612-1616, 2019.
Article in Chinese | WPRIM | ID: wpr-775676

ABSTRACT

OBJECTIVE@#To investigate the effects of quercetin on the apoptosis of platelets and to analyze the intrinsic mechanism.@*METHODS@#Firstly, the effects of quecetin on the apoptosis of platelets was detected by flow cytometry. Secondly, Western blot was used to detect the expression of apoptosis-related proteins in the platelets treated with quercetin for 2 and 4 day.@*RESULTS@#By flow cytometry, it was found that the apoptosis of platelets in the quercetin-treated group (2, 4 and 8 μmol/L) was inhibited, the apoptosis rate of platelets in 2, 4 and 8 μmol/L quercetin group was 3.12%±0.32%, 2.89%±0.15% and 2.31%±0.28%, respectively, which were signigicantly lover than that in control group (P<0.01). With the increase of quecetin concentration, the proportion ratio of platelets significantly decreased in a concentration-dependent manner(r=-0.9985). Similar results were observed on the 4th day. Western blot showed that the treatment with quercetin (2, 4 and 8 μmol/L) promoted the expression of anti-apoptotic protein BCL-2, inhibited the expression of pro-apoptotic protein BAX, resulting in a significant increase in the ratio of BCL-2/BAX (P<0.01), thereby inhibiting the apoptosis of platelets. Similar results were observed on the 4th day.@*CONCLUSION@#Quercetin can inhibit platelet apoptosis by increasing the ratio of apoptosis-related protein BCL-2/BAX in a concentration-dependent manner.


Subject(s)
Apoptosis , Apoptosis Regulatory Proteins , Blood Platelets , Quercetin
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