AIMTo compare the TAOC of quercetin, rutin, vitamin C, vitamin E in vitro and examine the effect of quercetin on TAOC of rat plasma after intragastric administration.

METHODSFe3+ reducing ability assay, UV spectrum analysis and HPLC analysis were used to measure TAOC of plasma and the contents of quercetin and rutin after intragastric administration.

RESULTSThe TAOC of quercetin was stronger than that of rutin and roughly equal to vitamin C and vitamin E in vitro. After intragastric administration of quercetin (40 mg/kg bw), the TAOC and content of quercetin in rat plasma increased significantly. Vitamin C also increased plasma TAOC significantly, but rutin and vitamin E didn't after intragastric administration. However, there was no remarkable absorption peak of quercetin on HPLC chromatograms and on the other hand, the peak areas of two unknown peaks near quercetin peak were increased after intragastric administration of quercetin.

CONCLUSIONThe antioxidant capacity of quercetin was stronger than rutin and comparable to vitamin C both in vitro and in vivo. After absorption, quercetin is metabolized to its derivatives.

Animals ; Antioxidants ; pharmacology ; Ascorbic Acid ; pharmacology ; Male ; Quercetin ; pharmacology ; Rats ; Rats, Wistar ; Rutin ; pharmacology ; Vitamin E ; pharmacology

The potential quality markers( Q-markers) of Eupatorium lindleyanum were studied with analytic hierarchy process(AHP)-entropy weight method(EWM) and network pharmacological method. Based on the concept of Q-markers of traditional Chinese medicine, AHP-EWM was employed to quantitatively identify the Q-markers of E. lindleyanum. AHP method was applied to the weight analysis of the validity, testability, and specificity of the first-level indexes, and EWM method was used to analyze the secondlevel indexes supported by literature and experimental data. At the same time, based on the theory and method of network pharmacology, the component-target-disease-efficacy network of E. lindleyanum was built, and the components most closely related to the efficacy of resolving phlegm and relieving cough and asthma were screened out. Through the integrated analysis of the results obtained with AHP-EWM and network pharmacological method, 13 compounds including rutin, quercetin, nepetin, cirsiliol, luteolin, hyperoside,isoquercitrin, kaempferol, caffeic acid, eupalinolide K, eupalinolide A, eupalinolide B, and eupalinolide C were comprehensively identified as the potential Q-markers of E. lindleyanum. The results provide a basis for the quality control of E. lindleyanum.
Analytic Hierarchy Process ; Drugs, Chinese Herbal ; Entropy ; Eupatorium ; Network Pharmacology ; Rutin

Rutin, a glycoside of flavonol, inhibits osteoclast formation induced by receptor activator of NF-kappaB ligand (RANKL) in bone marrow-derived macrophages. It reduces reactive oxygen species produced by RANKL and its inhibitory effect results from reduced levels of TNF-alpha Rutin also lowers NF-kappaB activation in response to RANKL.
Animals ; Mice ; Mice, Inbred C57BL ; NF-kappa B/*metabolism ; Osteoclasts/*cytology/*drug effects ; RANK Ligand/pharmacology ; Reactive Oxygen Species/*metabolism ; Rutin/*pharmacology ; Tumor Necrosis Factor-alpha/*metabolism/pharmacology

OBJECTIVETo explore the inhibitory effect and mechanism of rutin against platelet activating factor (PAF) induced platelet aggregation, 5-HT release and intra-platelet free calcium concentration.

METHODSThe rate of washed rabbit platelet (WRP) aggregation was measured by turbidimetry and O-phthaldialdehyde (OPT) fluoro-spectrophotometry (FSPM) was used to determine 5-HT content. The intraplatelet free calcium concentration was measured with Fura-2/AM FSPM assay.

RESULTSRutin in vitro was concentration-dependently inhibiting PAF (9.55 x 10(-9) mol/L) induced WRP aggregation, the IC50 of 5-HT release was 0.73, 1.13 mmol/L respectively and the intraplatelet free calcium concentration elevation evoked by PAF (4.78 x 10(-10) mol/L) were inhibited by 68.3, 136, 274, 545 mumol/L of rutin dose-dependently.

CONCLUSIONRutin could inhibit PAF induced platelet aggregation, 5-HT release and the increase of intraplatelet free calcium.

Animals ; Biological Transport, Active ; Blood Platelets ; metabolism ; Calcium ; metabolism ; Male ; Platelet Activating Factor ; antagonists & inhibitors ; Platelet Activation ; drug effects ; Platelet Aggregation Inhibitors ; pharmacology ; Rabbits ; Rutin ; pharmacology ; Serotonin ; metabolism

OBJECTIVETo compare the hemostatic effect of Flos Sophorae in crude, parched and carbonized forms and its extracts, including rutin, quercetin and tannin.

METHODSAll the testing samples were orally administered to the experimental animals for 5 days, then the bleeding time (BT), coagulation time (CT), platelet count and capillary permeability (CP) in the treated mice were tested, and the prothrombin time (PT), fibrinogen (FBG) content and platelet aggregation rate (PAR) in the treated rats were determined.

RESULTSAll the samples could lower the CP, BT and CT in mice and also decrease the plasma PT in rats. All three forms of Flos Sophorae could increase FBG in rats, while the three extracts of it could inhibit the PAR in rats obviously. In addition, rutin had the effect of raising the platelet count.

CONCLUSIONAll the three forms and three extracts of Flos Sophorae have hemostatic effect, the effect of parched and carbonized form is higher than that of crude drug. The mechanism of the hemostatic effect of the six kinds of sample might be various.

Animals ; Bleeding Time ; Blood Coagulation ; drug effects ; Capillary Permeability ; drug effects ; Drugs, Chinese Herbal ; chemistry ; pharmacology ; Female ; Flowers ; chemistry ; Hemostatics ; pharmacology ; Male ; Mice ; Quercetin ; isolation & purification ; pharmacology ; Rats ; Rats, Wistar ; Rutin ; isolation & purification ; pharmacology ; Sophora ; chemistry ; Tannins ; isolation & purification ; pharmacology

OBJECTIVETo evaluate the inhibitory effect of quercetin, rutin and puerarin on the LDL oxidation induced by Cu2+ and to investigate their action on the prevention and treatment of atherosclerosis.

METHODThe serum LDL was isolated by the one step density gradient ultracentrifugation. The LDL oxidation was induced by Cu2+ in vitro for different time periods. Quercetin, rutin and puerarin at 5 micromol x L(-1) were added respectively, as the experimental groups, 3 hours before oxidation. The oxidation of LDL in experimental and control groups was identified by measuring A234, REM, TBARS and protein carbonyls content, and the values were compared between the two groups.

RESULT(1) The values of A234, REM, TBARS and protein carbonyls formation increased gradually during LDL oxidation induced by Cu2+ in vitro. (2) During LDL oxidation induced by Cu2+ in vitro and incubation with each of quercetin, rutin and puerarin, the kinetic changes of A234, REM, TBARS and protein carbonyls formation showed lag phases of 2-6 h, 2 h and 2 h respectively, and the corresponding values for each of the agents treated group were reduced by 27.7%-49.6%, 24.1%-38.6%, 19.8%-34.3% and 36.4%-56.8%; 12.8%-39.3%, 15.7%-32.0%, 19.0%-28.1% and 12.8%-50.3%; and 3.3%-19.2%, 7.0%-22.5%, 19.5%-22.8% and 8.6%-47.0%, respectively.

CONCLUSIONThese results suggest that quercetin, rutin and puerarin can substantially inhibit LDL oxidation, and quercetin has antioxidation ability stronger than rutin and puerarin.

Antioxidants ; pharmacology ; Copper ; pharmacology ; Humans ; Isoflavones ; pharmacology ; Lipoproteins, LDL ; blood ; chemistry ; metabolism ; Oxidation-Reduction ; drug effects ; Protein Carbonylation ; drug effects ; Quercetin ; pharmacology ; Rutin ; pharmacology ; Thiobarbituric Acid Reactive Substances ; metabolism ; Time Factors

OBJECTIVETo determine the possible difference in vasodialtation effect of quercetin and rutin.

METHODSThe isolated rat thoracic aorta was treated with phenylephrine (PE), and the effects of quercetin and rutin on the preconstricted aorta rings with or without endothelium were determined by organ bath technique. Nitric oxide synthase inhibitor L-N(G)-nitroarginine methyl-ester (L-NAME), guanylyl cyclase inhibitor methylene blue, cyclooxygenase inhibitor indomethacin were used to explore the mechanism.

RESULTSQuercetin (10-160 micromol/L) caused vasorelaxation of aorta rings preconstricted with PE in endothelium-intact and denuded aorta rings in a dose-dependent manner. Rutin(10-160 micromol/L) caused dose-dependent vasorelaxation in endothelium-intact rings preconstricted with phenylephrine, but not in denuded aorta rings. The maximal response (Rmax) values calculated from vasorelaxation curves of quercetin and rutin were (77.20+/-6.11)% and (44.28+/-7.48)%, respectively. There was no difference between median effective concentration (EC(50)) values of quercetin and rutin. Pretreatment with L-NAME (0.1 mmol/L) abolished the vasorelaxation by rutin,but did not influence the vasodilating effect of quercetin in endothelium-intact rings. Pretreatment with methylene blue (10 mmol/L) canceled the vasorelaxation both by quercetin and rutin. Pretreatment with indomethacin (10 micromol/L) attenuated the vasodilatation of quercetin, but did not affect the vascular effect of rutin.

CONCLUSIONThe vasodilatation effect of quercetin is more potent than rutin. The vasodilatation effect of quercetin might be mediated by guanylyl cyclase and cyclooxygenase-dependent pathway, while the vasodilatation by rutin might be via nitric oxide-guanylyl cyclase pathway.

Animals ; Aorta, Thoracic ; drug effects ; Dose-Response Relationship, Drug ; Guanylate Cyclase ; metabolism ; In Vitro Techniques ; Male ; Nitric Oxide ; metabolism ; Phenylephrine ; pharmacology ; Prostaglandin-Endoperoxide Synthases ; metabolism ; Quercetin ; pharmacology ; Rats ; Rats, Sprague-Dawley ; Rutin ; pharmacology ; Vasodilator Agents ; pharmacology

OBJECTIVETo explore the protective effects of rutin against learning and memory impairment induced by trimethyltin (TMT) and investigate the possible mechanism.

METHODSForty 6- to 9-week-old male BALB/c mice were randomized equally into saline group (control), TMT group, TMT+rutin group, and rutin group. Mouse models of learning and memory impairment were establish by acute TMT (2.25 mg/kg) exposure. In TMT+rutin and rutin treatment groups, the mice received intraperitioneal injection of rutin (10 mg/kg) for 1 week before TMT exposure. Twenty-four hours after TMT exposure, Morris water maze test was employed to test the escape latency of the mice, and the synaptophysin expression in the hippocampus and cortex were analyzed by Western blotting.

RESULTSCompared that in TMT group, the escape latency of the mice in water maze test was significantly shorter in the other 3 groups (P<0.05); the escape latency in TMT +rutin group was similar with that in the control and rutin groups (P>0.05). Western blotting showed significantly decreased synaptophysin expression in the hippocampus and cortex in TMT group (P<0.05); synaptophysin expression in TMT +rutin group increased significantly compared with that in TMT group (P<0.05) but showed no statistical significance from that in rutin and control groups (P>0.05).

CONCLUSIONRutin pretreatment offers protective effect against TMT-induced learning and memory impairment in mice possibly by antagonizing decreased synaptophysin in the hippocampus and cortex.

Animals ; Cerebral Cortex ; drug effects ; metabolism ; Hippocampus ; drug effects ; metabolism ; Learning ; drug effects ; Male ; Memory Disorders ; chemically induced ; drug therapy ; Mice ; Mice, Inbred BALB C ; Neuroprotective Agents ; pharmacology ; Rutin ; pharmacology ; Synaptophysin ; metabolism ; Trimethyltin Compounds ; adverse effects

OBJECTIVETo investigate the protective effect of rutin against acute lung injury induced by lipopolysaccharide (LPS).

METHODSThirty C57BL/6 mice were randomly divided into control group, LPS-induced acute lung injury model group and treatment (LPS+Rutin) group. The pathological changes of the lung tissue were observed microscopically on paraffin sections with HE staining, and the lung wet/dry weight ratio was measured. The levels of TNF-α and IL-1β in the bronchoalveolar lavage fluid (BALF) were measured with ELISA, and the expressions of α-ENaC were detected with RT-PCR and Western blotting.

RESULTSPathological examination of the lung tissue revealed distinct inflammation, congestion and edema in the model group. The mice in the treatment group showed significantly milder lung injuries than those in the model group. Compared with the control group, the model group showed significantly increased lung wet/dry ratio and contents of TNF-α and IL-1β in BALF but lowered expressions of α-ENaC mRNA and protein. Compared with the model group, rutin treatment significantly decreased the lung wet/dry ratio and TNF-α and IL-1β levels in the BALF and increased the expressions of α-ENaC mRNA and protein.

CONCLUSIONRutin can inhibit the pulmonary inflammation and increase the expression of alveolar epithelial sodium channel protein to alleviate LPS-induced acute lung injury in mice.

Acute Lung Injury ; chemically induced ; drug therapy ; Animals ; Bronchoalveolar Lavage Fluid ; Epithelial Sodium Channels ; metabolism ; Interleukin-1beta ; metabolism ; Lipopolysaccharides ; Lung ; pathology ; Mice ; Mice, Inbred C57BL ; RNA, Messenger ; Rutin ; pharmacology ; Tumor Necrosis Factor-alpha ; metabolism

OBJECTIVEFlavonoids are present in foods such as fruits and vegetables. Several studies have demonstrated a relationship between the consumption of flavonoid-rich foods and prevention of human disease, including neurodegenerative disorders. We assessed the effect of rutin (quercetin-3-O-rutinoside) on oxidative stress in kainic acid (KA)-induced seizure.

METHODSThirty-six BALB/c mice were randomly divided into three groups. In the control group, saline (intra-peritoneal, i.p.) was administered for 7 d, and on the last day, KA (10 mg/kg, i.p.) was injected 30 min after administration of saline. In rutin groups, mice were pretreated with rutin (100 and 200 mg/kg, i.p.) for 7 d, and on the last day, KA (10 mg/kg, i.p.) was injected 30 min after administration of rutin. Subsequently, behavioural changes were observed in mice. Lipid peroxidation and oxidative stress were measured respectively in the early and late phases after KA-induced seizures.

RESULTSSeizure scores in the rutin groups were significantly lower than those in the control group (P < 0.01). Furthermore, rutin dose-dependently inhibited the number of wet-dog shakes (WDS) (P < 0.05). Malondialdehyde level in the hippocampus of the rutin groups was significantly lower than that in the hippocampus of the control group on days 1 and 21 after KA administration. In the rutin groups, the thiol levels observed on day 1 after KA administration were higher than that in the control group (P < 0.01).

CONCLUSIONThese results indicate that rutin has potential anticonvulsant and antioxidative activities against oxidative stress in KA-induced seizure in mice.

Animals ; Dose-Response Relationship, Drug ; Kainic Acid ; toxicity ; Lipid Peroxidation ; drug effects ; Male ; Mice ; Mice, Inbred BALB C ; Oxidative Stress ; drug effects ; Rutin ; pharmacology ; Seizures ; chemically induced ; metabolism ; Sulfhydryl Compounds ; analysis