The Experts below are selected from a list of 156 Experts worldwide ranked by ideXlab platform
Meili Guo - One of the best experts on this subject based on the ideXlab platform.
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autophagy is involved in the neuroprotective effect of Nicotiflorin
Journal of Ethnopharmacology, 2021Co-Authors: Yeqing Wang, Shanshan Zhang, Yanjie Zhang, Xiaodong Yan, Yue Gao, Wenzheng Wang, Chong Liu, Meili GuoAbstract:Abstract Ethnopharmacological relevance Nicotiflorin is a flavonoid glycoside derived from the traditional Chinese medicine FlosCarthami, dried petals of Carthamus tinctorius L., and has been confirmed to be a promising novel drug candidate for ischemic stroke. Yet, the exact role of Nicotiflorin in cerebral I/R injury is uncharacterized and the possible mechanisms have not been clearly expounded. Aim of the study The present study was designed to determine the effect of Nicotiflorin on cerebral ischemia/reperfusion (I/R) injury and its relationship with autophagy. Materials and methods Middle cerebral artery occlusion (MCAO) in rats and oxygen-glucose deprivation and reintroduction (OGD/R) in SH-SY5Y cells were established in in vivo and in vitro models, respectively. The severity of MCAO was assessed by brain infarct size, neurological scores and survival rate. The severity of OGD/R was evaluated by cell viability, lactate dehydrogenase (LDH) release and cell apoptosis. The level of autophagy was evaluated both in vivo and in vitro. Autophagosomes were observed using transmission electron microscopy and autophagic flux was measured using mRFP-GFP-tandem fluorescent LC3 adenovirus. Autophagy-related proteins (LC3-II/I, SQSTM1, beclin-1, Phospho-mTOR/mTOR) were measured by immunoblot. Autophagy-related mRNA levels (Becn1, Atg7) were detected by Real-Time PCR. Inhibition of autophagy was implemented by 3-Methyladenine (3-MA) or chloroquine in vitro. Results In vivo, Nicotiflorin treatment alleviated brain damage and neurological deficit while it dramatically increased 72 h survival rate in rats. In vitro, Nicotiflorin treatment also ameliorated the severity of OGD/R. Moreover, Nicotiflorin treatment increased ischemic penumbra autophagy (autophagosomes, BECN1, LC3-II/I ratio, SQSTM1, Phospho-mTOR/mTOR, Atg7). In vitro, Nicotiflorin likewise enhanced autophagy and promoted autophagy flux. Furthermore, the blockade of autophagy by 3-MA or chloroquine disabled the efficacic of Nicotiflorin in preventing cell damage upon OGD/R insult. Conclusion These findings suggest that autophagy plays a significant role in the protective effect of Nicotiflorin against ischemic stroke.
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protective effects of Nicotiflorin on reducing memory dysfunction energy metabolism failure and oxidative stress in multi infarct dementia model rats
Pharmacology Biochemistry and Behavior, 2007Co-Authors: Jinling Huang, Meili Guo, Yuanying Jiang, Yongbing Cao, Yan WangAbstract:Abstract The present study aimed to determine whether Nicotiflorin, a natural flavonoid extracted from coronal of Carthamus tinctorius , has a protective effect on cerebral multi-infarct dementia in rats. The multi-infarct dementia model rats were prepared by injecting man-made micro-thrombi into the right hemisphere. The administration groups were treated once daily with 30, 60 and 120 mg/kg Nicotiflorin (i.g.) from 5 days before ischemia operation to 3 days after the operation for biochemical examination, 10 days for Morris water maze study and morphological observations and 20 days for eight-arm radial maze task. 2,3,5-triphenyltetrazolium chloride (TTC) staining showed that infarct volume of each Nicotiflorin administration group was much smaller than that of vehicle-treated multi-infarct dementia group, and hematoxylin and eosin (HE) staining showed that histopathological abnormalities of each Nicotiflorin group were also much lighter than that of vehicle-treated multi-infarct dementia group. Each Nicotiflorin group showed much better spatial memory performance in Morris water maze tests and eight-arm radial maze task compared with the vehicle-treated multi-infarct dementia group, significantly attenuated the elevation of lactic acid and malondialdehyde (MDA) contents and the decrease in lactate dehydrogenase (LDH), Na + K + ATPase, Ca 2+ Mg 2+ ATPase and superoxide dismutase (SOD) activity in the brain tissue which was composed of striatum, cortex and hippocampus of the ischemia hemisphere at day 3 after ischemia operation. These results suggest that Nicotiflorin has protective effects on reducing memory dysfunction, energy metabolism failure and oxidative stress in multi-infarct dementia model rats.
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neuroprotection of Nicotiflorin in permanent focal cerebral ischemia and in neuronal cultures
Biological & Pharmaceutical Bulletin, 2006Co-Authors: Meili Guo, Ge ZhangAbstract:Nicotiflorin is a single component extracted from traditional Chinese medicine Flos Carthami. In this study, we investigated its neuroprotection in permanent focal cerebral ischemia model in rats, and in an in vitro model of ischemia. At doses of 2.5, 5 and 10 mg/kg, Nicotiflorin administered immediately after the onset of ischemia markedly reduced brain infarct volume and neurological deficits. For primarily cultured neurons suffered 2 h hypoxia followed by 24 h reoxygenation, Nicotiflorin significantly attenuated cell death and reduced LDH release. Morphological observation also directly confirmed its protective effect on neuron. These results provided strong pharmacological basis for its potential therapeutic role in cerebral ischemic illness.
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Nicotiflorin reduces cerebral ischemic damage and upregulates endothelial nitric oxide synthase in primarily cultured rat cerebral blood vessel endothelial cells
Journal of Ethnopharmacology, 2006Co-Authors: Meili Guo, Ge ZhangAbstract:Abstract Nicotiflorin is a flavonoid glycoside extracted from a traditional Chinese medicine Flos Carthami. In the current study, we investigated the neuroprotective effect of Nicotiflorin on a transient focal cerebral ischemia–reperfusion model in rats. Nicotiflorin (2.5–10 mg/kg) administered after onset of ischemia markedly reduced brain infarct volume by 24.5–63.2% and neurological deficits. Also the effect of Nicotiflorin on endothelial nitric oxide synthase (eNOS) activity, mRNA and protein expression after hypoxia–reoxygenation (H–R) treatment was investigated in an in vitro model mimic cerebrum ischemia–reperfusion in vivo. After total 4 h hypoxia and 12 h reoxygenation, eNOS activity, mRNA and protein levels in the primarily cultured rat cerebral blood vessel endothelial cells treated with Nicotiflorin (25–100 μg/ml) 2 h after onset of hypoxia were significantly higher than eNOS activity, mRNA and protein levels in the pure H–R cells and also higher than eNOS activity, mRNA and protein levels in cells cultured under normoxic conditions. The results demonstrated that Nicotiflorin had a protective effect against cerebral ischemic damage. The results also gave an important elucidation for the mechanism underlying the protective effect at the cellular level.
Chengchang Chen - One of the best experts on this subject based on the ideXlab platform.
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five secoiridoid glucosides from fraxinus formosana
Phytochemistry, 1992Co-Authors: Takao Tanahashi, Tetsuro Fujita, Naotaka Nagakura, Kenichiro Inoue, Atsuko Itoh, Hiroko Watanabe, Chengchang ChenAbstract:Abstract Five new secoiridoid glucosides, formoside, 1‴- O -β- d -glucosylformoside, 1‴ - O -β- d -glucosylfraxiformoside, isoligustrosidic acid and framoside, were isolated from Fraxinus formosana , together with the known glycosides, 8-epikingiside, benzyl- O -β- d -glucoside and Nicotiflorine. The structural elucidation of these glucosides by spectroscopic and chemical studies is described.
Dae-won Chung - One of the best experts on this subject based on the ideXlab platform.
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isolation and anti inflammatory effect of astragalin synthesized by enzymatic hydrolysis of tea seed extract
Journal of the Science of Food and Agriculture, 2011Co-Authors: Sang-jae Park, Sang-gu Bang, Dae-won ChungAbstract:BACKGROUND: The application of tea seed extract (TSE) has been widely investigated because of its biological activities. In this paper, two flavonol triglycosides in TSE—camelliaside A (CamA) and camelliaside B (CamB)—were subjected to hydrolysis in the presence of two commercial enzyme complexes (Pectinex™ series): Smash and Mash. RESULTS: Smash hydrolyzed only the xylosyl moiety of CamB, and the main product was kaempferol diglycoside (Nicotiflorin, NF). On the other hand, Mash induced the hydrolysis of both CamA and CamB, and kaempferol monoglycoside (astragalin, AS) was found to be a main product. Pure AS with > 96% purity was prepared by enzymatic hydrolysis of TSE using Mash, and the chemical structure of AS was confirmed by 1H- and 13C-nuclear magnetic resonance analyses. The prepared pure AS showed anti-inflammatory activities by significantly inhibiting cellular nitrite oxide (IC50 = 363 µg mL−1), prostaglandin E2 (IC50 = 134 µg mL−1) and interleukin-6 production (IC50 = 289 µg mL−1) by lipopolysaccharide -stimulated RAW 264.7 cells. CONCLUSION: It was concluded that pure AS can be prepared by enzymatic partial hydrolysis of TSE and employed as an anti-inflammatory material. This is the first study to address the preparation of pure AS from natural sources. Copyright © 2011 Society of Chemical Industry
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isolation and characterization of Nicotiflorin obtained by enzymatic hydrolysis of two precursors in tea seed extract
Journal of Agricultural and Food Chemistry, 2010Co-Authors: Hyangbok Lee, Sang-jae Park, Sang-gu Bang, Eunki Kim, Tae Gil Kim, Dae-won ChungAbstract:Two flavonol triglycosides, camelliaside A (CamA) and camelliaside B (CamB), of tea seed extract (TSE) were subjected to enzymatic hydrolysis. Among five kinds of glycosidases investigated, β-galactosidase (Gal) induced selective hydrolysis of CamA. On the other hand, pectinase (Pec) and cellulase (Cel) induced hydrolysis of CamB. For Gal and Pec, only kaempferol diglycoside (Nicotiflorin, NF) was produced; on the other hand, significant amounts of kaempferol monoglycoside (astragalin, AS) and kaempferol (KR) were also detected for Cel. The combination of the use of Gal and Pec in the enzymatic hydrolysis of TSE afforded NF with high specificity. Crude NF with 22% purity was recovered from the enzymatic reaction mixture by extraction with organic solvent, and pure NF with >95% purity was obtained by crystallized in water. The chemical structure of NF was confirmed by 1H and 13C NMR analyses.
Florence Val - One of the best experts on this subject based on the ideXlab platform.
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Nicotiflorin rutin and chlorogenic acid phenylpropanoids involved differently in quantitative resistance of potato tubers to biotrophic and necrotrophic pathogens
Plant Physiology and Biochemistry, 2012Co-Authors: Alexander Kroner, Nathalie Marnet, Didier Andrivon, Florence ValAbstract:Physiological and molecular mechanisms underlying quantitative resistance of plants to pathogens are still poorly understood, but could depend upon differences in the intensity or timing of general defense responses. This may be the case for the biosynthesis of phenolics which are known to increase after elicitation by pathogens. We thus tested the hypothesis that differences in quantitative resistance were related to differential induction of phenolics by pathogen-derived elicitors. Five potato cultivars (Solanum tuberosum, L.) spanning a range of quantitative resistance were treated with a concentrated culture filtrate (CCF) of Phytophthora infestans or purified lipopolysaccharides (LPS) from Pectobacterium atrosepticum. The kinetic of phenolics accumulation was followed and a set of typical phenolics was identified: chlorogenic acid, phenolamides and flavonols including rutin (quercetin-3-O-rutinoside) and Nicotiflorin (kaempferol-3-O-rutinoside). Our results showed that CCF but not LPS induced differential accumulation of major phenolics among cultivars. Total phenolics were related with resistance to P. atrosepticum but not to P. infestans. However, Nicotiflorin was inversely related with resistance to both pathogens. Rutin, but not Nicotiflorin, inhibited pathogen growth in vitro at physiological concentrations. These data therefore suggest that (i) several phenolics are candidate markers for quantitative resistance in potato, (ii) some of these are pathogen specific although they are produced by a general defense pathway, (iii) resistance marker molecules do not necessarily have antimicrobial activity, and (iv) the final content of these target molecules-either constitutive or induced-is a better predictor of resistance than their inducibility by pathogen elicitors.
Wei Zhang - One of the best experts on this subject based on the ideXlab platform.
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Nicotiflorin attenuates cell apoptosis in renal ischemia reperfusion injury through activating transcription factor 3
Nephrology, 2021Co-Authors: Lin Wang, Chen Guan, Yue Zhang, Chengyu Yang, Long Zhao, Hong Luan, Bin Zhou, Lin Che, Yanfei Wang, Wei ZhangAbstract:INTRODUCTION Nicotiflorin is the main characteristic component of Nymphaea candida, which is a natural product that reportedly ameliorates acute injury of the liver and cerebral cortex, but the effect of Nicotiflorin on acute kidney injury (AKI) remains unknown. This study aimed to investigate the effects of Nicotiflorin on ischaemia/reperfusion (I/R) AKI and the associated mechanisms. METHODS We performed both (a) in vivo experiments with C57BL/6 mice with bilateral renal pedicles clamped for 45 minutes and (b) in vitro experiments with human kidney epithelial cells (HK-2) exposed to hypoxia/reoxygenation to mimic I/R injury to study the role of Nicotiflorin in AKI. RESULTS In vivo, Nicotiflorin administration exerted protective effects on renal injury, as demonstrated by reductions in the levels of caspase3 and Bad (P < .05), the upregulation of Bcl-2 expression (P < .05) and improved renal histologic changes, which suggested that Nicotiflorin can alleviate I/R injury and cell apoptosis. In vitro, Nicotiflorin at a concentration of 75 μg/mL protected cells from hypoxia, which further confirmed that Nicotiflorin exerts beneficial effects on hypoxia/reoxygenation. Through computational molecular docking, we found that activating transcription factor 3 (ATF3) exhibits a robust interaction with Nicotiflorin with a simulated binding energy of -9.2°. We verified the interaction of Nicotiflorin with ATF3 in HK-2 cells, and found that Nicotiflorin reduced the apoptosis of HK-2 through ATF3. CONCLUSION Based on the above-described results, Nicotiflorin appears to have a beneficial impact on deteriorated renal function, as demonstrated using an experimental I/R model. The underlying mechanisms of Nicotiflorin might inhibit HK-2 cell apoptosis through ATF3.