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Ruichang Gao - One of the best experts on this subject based on the ideXlab platform.
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absorption metabolism and bioactivity of Vitexin recent advances in understanding the efficacy of an important nutraceutical
Critical Reviews in Food Science and Nutrition, 2021Co-Authors: Ye Peng, Ruichang Gao, Ren-you Gan, Mingxuan Yang, David Julian Mcclements, Quancai SunAbstract:Vitexin, an apigenin-8-C-glucoside, is widely present in numerous edible and medicinal plants. Vitexin possesses a variety of bioactive properties, including antioxidation, anti-inflammation, anti-...
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Absorption, metabolism, and bioactivity of Vitexin: recent advances in understanding the efficacy of an important nutraceutical
Critical reviews in food science and nutrition, 2020Co-Authors: Ye Peng, Ruichang Gao, Ren-you Gan, Mingxuan Yang, David Julian Mcclements, Quancai SunAbstract:Vitexin, an apigenin-8-C-glucoside, is widely present in numerous edible and medicinal plants. Vitexin possesses a variety of bioactive properties, including antioxidation, anti-inflammation, anti-cancer, neuron-protection, and cardio-protection. Other beneficial health effects, such as fat reduction, glucose metabolism, and hepatoprotection, have also been reported in recent studies. This review briefly discusses the absorption and metabolism of Vitexin, as well as its influence on gut microbiota. Recent advances in understanding the pharmacological and biological effects of Vitexin are then reviewed. Improved knowledge of the absorption, metabolism, bioactivity, and molecular targets of Vitexin is crucial for the better utilization of this emerging nutraceutical as a chemopreventive and chemotherapeutic agent.
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Vitexin ameliorates high fat diet induced obesity in male c57bl 6j mice via the ampkα mediated pathway
Food & Function, 2019Co-Authors: Ye Peng, Quancai Sun, Wengang Jin, Li Yuan, Ruichang GaoAbstract:Vitexin, a bioactive compound isolated from hawthorn leaf extracts, has been reported to exhibit many biological activities, such as anticancer, antioxidation, and adipogenesis inhibition activities. The current study explored the effects of Vitexin on high fat diet (HFD)-induced obesity/adipogenesis in male C57BL/6J mice and 3T3-L1 adipocytes, as well as the underlying mechanisms thereof. Vitexin significantly mitigated HFD-induced body weight gain and adiposity. Vitexin also partially normalized serum, hepatic lipid contents, and decreased adipocyte size induced by the HFD. Consistently, there were significant effects of Vitexin on important regulators of lipid metabolism, including AMP-activated protein kinase-α (AMPKα), CAATT element binding protein-α (C/EBPα), and fatty acid synthase (FAS) in white adipose tissue. Moreover, Vitexin significantly inhibited fat accumulation in 3T3-L1 adipocytes, and this was totally abolished by compound C (an AMPKα inhibitor). These results suggest that Vitexin may prevent HFD-induced obesity/adipogenesis via the AMPKα mediated pathway.
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Vitexin ameliorates high fat diet-induced obesity in male C57BL/6J mice via the AMPKα-mediated pathway
Food & function, 2019Co-Authors: Ye Peng, Quancai Sun, Wengang Jin, Li Yuan, Ruichang GaoAbstract:Vitexin, a bioactive compound isolated from hawthorn leaf extracts, has been reported to exhibit many biological activities, such as anticancer, antioxidation, and adipogenesis inhibition activities. The current study explored the effects of Vitexin on high fat diet (HFD)-induced obesity/adipogenesis in male C57BL/6J mice and 3T3-L1 adipocytes, as well as the underlying mechanisms thereof. Vitexin significantly mitigated HFD-induced body weight gain and adiposity. Vitexin also partially normalized serum, hepatic lipid contents, and decreased adipocyte size induced by the HFD. Consistently, there were significant effects of Vitexin on important regulators of lipid metabolism, including AMP-activated protein kinase-α (AMPKα), CAATT element binding protein-α (C/EBPα), and fatty acid synthase (FAS) in white adipose tissue. Moreover, Vitexin significantly inhibited fat accumulation in 3T3-L1 adipocytes, and this was totally abolished by compound C (an AMPKα inhibitor). These results suggest that Vitexin may prevent HFD-induced obesity/adipogenesis via the AMPKα mediated pathway.
Liuyi Dong - One of the best experts on this subject based on the ideXlab platform.
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Vitexin attenuates myocardial ischemia reperfusion injury in rats by regulating mitochondrial dysfunction induced by mitochondrial dynamics imbalance
Biomedicine & Pharmacotherapy, 2020Co-Authors: Wei Xue, Xin Wang, Hong Tang, Fanfan Sun, Huaqing Zhu, Dake Huang, Liuyi DongAbstract:Vitexin (VT) is a main bioactive flavonoid compound derived from the dried leaf of hawthorn (Crataegus pinnatifida), a widely used Chinese traditional folk medicine. Recent studies have shown that Vitexin presents cardioprotective effects in vivo and in vitro. Mitochondrial dysfunction is a salient feature of myocardial ischemia/reperfusion (I/R) injury (MIRI), but the potential mechanism is still unclear. This study investigated the cardioprotective effect of Vitexin against MIRI and its possible mechanism. Isolated SD rat hearts were subjected to MIRI in a Langendorff perfusion system, and H9c2 cells were subjected to hypoxia/reoxygenation (H/R) in vitro. Ex vivo experiments showed improved left ventricular function and reduced infarct size in the Vitexin group. Transmission electron microscopy showed that I/R caused outer mitochondrial membrane rupture, cristae disappearance and vacuolation, while Vitexin reduced mitochondrial damage and ultimately reduced cardiomyocyte apoptosis. In vitro, Vitexin protected H9c2 cells from H/R-induced mitochondrial dysfunction, significantly reducing ROS levels; improving mitochondrial activity, mitochondrial membrane potential and ATP content; markedly increasing MFN2 expression and reducing the recruitment of Drp1 in mitochondria. These results suggest a new protective mechanism of Vitexin for ischemic heart disease treatment.
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Vitexin attenuates myocardial ischemia/reperfusion injury in rats by regulating mitochondrial dysfunction induced by mitochondrial dynamics imbalance.
Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie, 2020Co-Authors: Wei Xue, Xin Wang, Hong Tang, Fanfan Sun, Huaqing Zhu, Dake Huang, Liuyi DongAbstract:Vitexin (VT) is a main bioactive flavonoid compound derived from the dried leaf of hawthorn (Crataegus pinnatifida), a widely used Chinese traditional folk medicine. Recent studies have shown that Vitexin presents cardioprotective effects in vivo and in vitro. Mitochondrial dysfunction is a salient feature of myocardial ischemia/reperfusion (I/R) injury (MIRI), but the potential mechanism is still unclear. This study investigated the cardioprotective effect of Vitexin against MIRI and its possible mechanism. Isolated SD rat hearts were subjected to MIRI in a Langendorff perfusion system, and H9c2 cells were subjected to hypoxia/reoxygenation (H/R) in vitro. Ex vivo experiments showed improved left ventricular function and reduced infarct size in the Vitexin group. Transmission electron microscopy showed that I/R caused outer mitochondrial membrane rupture, cristae disappearance and vacuolation, while Vitexin reduced mitochondrial damage and ultimately reduced cardiomyocyte apoptosis. In vitro, Vitexin protected H9c2 cells from H/R-induced mitochondrial dysfunction, significantly reducing ROS levels; improving mitochondrial activity, mitochondrial membrane potential and ATP content; markedly increasing MFN2 expression and reducing the recruitment of Drp1 in mitochondria. These results suggest a new protective mechanism of Vitexin for ischemic heart disease treatment.
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Vitexin protects brain against ischemia reperfusion injury via modulating mitogen activated protein kinase and apoptosis signaling in mice
Phytomedicine, 2015Co-Authors: Yanan Wang, Zhiwu Chen, Yilan Zhen, Qin Jiang, Gongliang Zhang, Liuyi DongAbstract:Vitexin is a major bioactive flavonoid compound derived from the dried leaf of hawthorn (Crataegus pinnatifida), a widely used conventional folk medicine in China. Recent studies have shown that Vitexin presents neuroprotective effects in vitro. Whether this protective effect applies to the cerebral ischemia/reperfusion (I/R) injury remains elusive. In the present study, we examined the potential neuroprotective effect of Vitexin against cerebral I/R injury and underlying mechanisms. A focal cerebral I/R model in male Kunming mice was induced by middle cerebral artery occlusion (MCAO) for 2 h followed by reperfusion for 22 h. The neurological function and infarct volume were assessed by using Long's five-point scale system and triphenyl-tetrazolium chloride (TTC) staining technique, respectively. Neuronal damage was evaluated by histological staining. Extracellular signal-regulated kinases 1/2 (ERK1/2), c-Jun N-terminal kinases (JNK) and p38 phosphorylation, and apoptosis were measured via Western blot at 24 h after reperfusion. As a result, systemic Vitexin treatment significantly reduced neurological deficit, cerebral infarct volume and neuronal damage when compared with the I/R group. Western blot analyses revealed that Vitexin markedly upregulated p-ERK1/2 and downregulated p-JNK and p-p38. Meanwhile, Vitexin increased Bcl-2 expression and suppressed the overexpression of Bax in the I/R injury mice. In conclusion, the results indicate that Vitexin protects brain against cerebral I/R injury, and this effect may be regulated by mitogen-activated protein kinase (MAPK) and apoptosis signaling pathways.
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Vitexin protects against myocardial ischemia reperfusion injury in langendorff perfused rat hearts by attenuating inflammatory response and apoptosis
Food and Chemical Toxicology, 2011Co-Authors: Liuyi Dong, Yifei Fan, Xu Shao, Zhiwu ChenAbstract:The aim of the present study is to investigate the effects and its possible underlying mechanisms of Vitexin on myocardial ischemia/reperfusion (I/R) injury in isolated rat hearts. Isolated rat hearts were perfused with Langendorff apparatus, which subjected to 30 min ischemia and then followed by 60 min reperfusion. In the isolated rat heart subjected to I/R injury, treatment of Vitexin (50, 100, 200 μmol/L) significantly enhanced coronary flow, and decreased the pathological scores of myocardium. 50, 100, 200 μmol/L Vitexin significantly attenuated I/R-induced increases of myocardial TNF-α and IL-1β, and 25, 50, 100, 200 μmol/L Vitexin significantly reduced apoptosis index of cardiac muscle cell of rat isolated heart subjected to I/R injury. Vitexin significantly inhibited I/R-induced increase of myocardial Bax protein expression; however, 100, 200 μmol/L Vitexin markedly increased myocardial Bcl-2 protein expression. Furthermore, Vitexin at concentrations of 50, 100, 200 μmol/L significantly reduced expression of myocardial NF-κBp65 protein. Therefore, these results demonstrate that Vitexin exhibits significant protective effect against myocardial I/R injury in isolated rat heart, which is related to inhibition of the release of inflammatory cytokines and the apoptosis of cardiac muscle cell via up-regulating protein expression of Bcl-2 as well as down-regulating Bax and NF-κBp65.
Xing Tang - One of the best experts on this subject based on the ideXlab platform.
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simultaneous determination of Vitexin 4 o glucoside Vitexin 2 o rhamnoside rutin and Vitexin from hawthorn leaves flavonoids in rat plasma by uplc esi ms ms
Journal of Chromatography B, 2010Co-Authors: Wenjun Zhang, Guofeng Zhang, Xing TangAbstract:Abstract A sensitive and accurate ultra-performance liquid chromatography electrospray ionization tandem mass spectrometry (UPLC–ESI-MS/MS) method was developed and validated for the simultaneous determination of Vitexin-4″-O-glucoside (VGL), Vitexin-2″-O-rhamnoside (VRH), rutin (RUT) and Vitexin (VIT) in rat plasma after intravenous administration of hawthorn leaves flavonoids (HLF). Following protein precipitation by methanol, the analytes were separated on an ACQUITY UPLC BEH C 18 column packed with 1.7 μm particles by gradient elution using a mobile phase composed of acetonitrile and water (containing 0.1% formic acid) at a flow rate of 0.20 mL/min. The analytes and diphenhydramine (internal standard, IS) were detected in the multiple reaction monitoring (MRM) mode by means of an electrospray ionization (ESI) interface ( m / z 292.96 for Vitexin-4″-O-glucoside, m / z 293.10 for Vitexin-2″-O-rhamnoside, m / z 299.92 for rutin, m / z 310.94 for Vitexin and m / z 166.96 for IS). The calibration curve was linear over the range 10–40,000 ng/mL for Vitexin-4″-O-glucoside, 10–50,000 ng/mL for Vitexin-2″-O-rhamnoside, 8–1000 ng/mL for rutin and 16–2000 ng/mL for Vitexin. The intra- and inter-run precisions (relative standard deviation, RSD) of these analytes were all within 15% and the accuracy (the relative error, RE) ranged from −10% to 10%. The stability experiment indicated that the four analytes in rat plasma samples and plasma extracts under anticipated conditions were stable. The developed method was applied for the first time to pharmacokinetic studies of the four bioactive compounds of hawthorn leaves flavonoids following a single intravenous administration of 20 mg/kg in rats.
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Simultaneous determination of Vitexin-4″-O-glucoside, Vitexin-2″-O-rhamnoside, rutin and Vitexin from hawthorn leaves flavonoids in rat plasma by UPLC-ESI-MS/MS.
Journal of chromatography. B Analytical technologies in the biomedical and life sciences, 2010Co-Authors: Wenjun Zhang, Guofeng Zhang, Xing TangAbstract:Abstract A sensitive and accurate ultra-performance liquid chromatography electrospray ionization tandem mass spectrometry (UPLC–ESI-MS/MS) method was developed and validated for the simultaneous determination of Vitexin-4″-O-glucoside (VGL), Vitexin-2″-O-rhamnoside (VRH), rutin (RUT) and Vitexin (VIT) in rat plasma after intravenous administration of hawthorn leaves flavonoids (HLF). Following protein precipitation by methanol, the analytes were separated on an ACQUITY UPLC BEH C 18 column packed with 1.7 μm particles by gradient elution using a mobile phase composed of acetonitrile and water (containing 0.1% formic acid) at a flow rate of 0.20 mL/min. The analytes and diphenhydramine (internal standard, IS) were detected in the multiple reaction monitoring (MRM) mode by means of an electrospray ionization (ESI) interface ( m / z 292.96 for Vitexin-4″-O-glucoside, m / z 293.10 for Vitexin-2″-O-rhamnoside, m / z 299.92 for rutin, m / z 310.94 for Vitexin and m / z 166.96 for IS). The calibration curve was linear over the range 10–40,000 ng/mL for Vitexin-4″-O-glucoside, 10–50,000 ng/mL for Vitexin-2″-O-rhamnoside, 8–1000 ng/mL for rutin and 16–2000 ng/mL for Vitexin. The intra- and inter-run precisions (relative standard deviation, RSD) of these analytes were all within 15% and the accuracy (the relative error, RE) ranged from −10% to 10%. The stability experiment indicated that the four analytes in rat plasma samples and plasma extracts under anticipated conditions were stable. The developed method was applied for the first time to pharmacokinetic studies of the four bioactive compounds of hawthorn leaves flavonoids following a single intravenous administration of 20 mg/kg in rats.
Jingyao Liu - One of the best experts on this subject based on the ideXlab platform.
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Vitexin attenuates lipopolysaccharide-induced acute lung injury by controlling the Nrf2 pathway
PloS one, 2018Co-Authors: Jingyao LiuAbstract:A major feature of acute lung injury (ALI) is excessive inflammation in the lung. Vitexin is an active component from medicinal plants which has antioxidant and anti-inflammatory activities. Oxidative stress and inflammation play important roles in the pathophysiological processes in ALI. In the current study, we investigate the effect and potential mechanisms of Vitexin on lipopolysaccharide (LPS)-induced ALI. ALI was induced by LPS intratracheal instillation in C57BL/6 wild-type mice and Nrf2 gene knocked down (Nrf2-/-) mice. One hour before LPS challenge, Vitexin or vehicle intraperitoneal injection was performed. Bronchoalveolar lavage fluid and lung tissues were examined for lung inflammation and injury at 24 h after LPS challenge. Our animal study's results showed that LPS-induced recruitment of neutrophils and elevation of proinflammatory cytokine levels were attenuated by Vitexin treatment. Vitexin decreased lung edema and alveolar protein content. Moreover, Vitexin activated nuclear factor erythroid-2-related factor 2 (Nrf2), and increased the activity of its target gene heme oxygenase (HO)-1. The LPS-induced reactive oxygen species were inhibited by Vitexin. In addition, the activation of the nucleotide-binding domain and leucine-rich repeat PYD-containing protein 3 (NLRP3) inflammasome was suppressed by Vitexin. However, these effects of Vitexin were abolished in the Nrf2-/- mice. Our cell studies showed that Vitexin enhanced the expression of Nrf2 and HO-1 activity. Moreover, reactive oxygen species (ROS) and IL-1β productions were reduced in Vitexin-treated cells. However, knockdown of Nrf2 by siRNA in RAW cells reversed the benefit of Vitexin. Vitexin suppresses LPS-induced ALI by controlling Nrf2 pathway.
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Vitexin attenuates lipopolysaccharide induced acute lung injury by controlling the nrf2 pathway
PLOS ONE, 2018Co-Authors: Jingyao LiuAbstract:Background A major feature of acute lung injury (ALI) is excessive inflammation in the lung. Vitexin is an active component from medicinal plants which has antioxidant and anti-inflammatory activities. Oxidative stress and inflammation play important roles in the pathophysiological processes in ALI. In the current study, we investigate the effect and potential mechanisms of Vitexin on lipopolysaccharide (LPS)-induced ALI. Methods ALI was induced by LPS intratracheal instillation in C57BL/6 wild-type mice and Nrf2 gene knocked down (Nrf2-/-) mice. One hour before LPS challenge, Vitexin or vehicle intraperitoneal injection was performed. Bronchoalveolar lavage fluid and lung tissues were examined for lung inflammation and injury at 24 h after LPS challenge. Results Our animal study’s results showed that LPS-induced recruitment of neutrophils and elevation of proinflammatory cytokine levels were attenuated by Vitexin treatment. Vitexin decreased lung edema and alveolar protein content. Moreover, Vitexin activated nuclear factor erythroid-2-related factor 2 (Nrf2), and increased the activity of its target gene heme oxygenase (HO)-1. The LPS-induced reactive oxygen species were inhibited by Vitexin. In addition, the activation of the nucleotide-binding domain and leucine-rich repeat PYD-containing protein 3 (NLRP3) inflammasome was suppressed by Vitexin. However, these effects of Vitexin were abolished in the Nrf2-/- mice. Our cell studies showed that Vitexin enhanced the expression of Nrf2 and HO-1 activity. Moreover, reactive oxygen species (ROS) and IL-1β productions were reduced in Vitexin-treated cells. However, knockdown of Nrf2 by siRNA in RAW cells reversed the benefit of Vitexin. Conclusions Vitexin suppresses LPS-induced ALI by controlling Nrf2 pathway.
Ye Peng - One of the best experts on this subject based on the ideXlab platform.
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absorption metabolism and bioactivity of Vitexin recent advances in understanding the efficacy of an important nutraceutical
Critical Reviews in Food Science and Nutrition, 2021Co-Authors: Ye Peng, Ruichang Gao, Ren-you Gan, Mingxuan Yang, David Julian Mcclements, Quancai SunAbstract:Vitexin, an apigenin-8-C-glucoside, is widely present in numerous edible and medicinal plants. Vitexin possesses a variety of bioactive properties, including antioxidation, anti-inflammation, anti-...
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Absorption, metabolism, and bioactivity of Vitexin: recent advances in understanding the efficacy of an important nutraceutical
Critical reviews in food science and nutrition, 2020Co-Authors: Ye Peng, Ruichang Gao, Ren-you Gan, Mingxuan Yang, David Julian Mcclements, Quancai SunAbstract:Vitexin, an apigenin-8-C-glucoside, is widely present in numerous edible and medicinal plants. Vitexin possesses a variety of bioactive properties, including antioxidation, anti-inflammation, anti-cancer, neuron-protection, and cardio-protection. Other beneficial health effects, such as fat reduction, glucose metabolism, and hepatoprotection, have also been reported in recent studies. This review briefly discusses the absorption and metabolism of Vitexin, as well as its influence on gut microbiota. Recent advances in understanding the pharmacological and biological effects of Vitexin are then reviewed. Improved knowledge of the absorption, metabolism, bioactivity, and molecular targets of Vitexin is crucial for the better utilization of this emerging nutraceutical as a chemopreventive and chemotherapeutic agent.
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Vitexin ameliorates high fat diet induced obesity in male c57bl 6j mice via the ampkα mediated pathway
Food & Function, 2019Co-Authors: Ye Peng, Quancai Sun, Wengang Jin, Li Yuan, Ruichang GaoAbstract:Vitexin, a bioactive compound isolated from hawthorn leaf extracts, has been reported to exhibit many biological activities, such as anticancer, antioxidation, and adipogenesis inhibition activities. The current study explored the effects of Vitexin on high fat diet (HFD)-induced obesity/adipogenesis in male C57BL/6J mice and 3T3-L1 adipocytes, as well as the underlying mechanisms thereof. Vitexin significantly mitigated HFD-induced body weight gain and adiposity. Vitexin also partially normalized serum, hepatic lipid contents, and decreased adipocyte size induced by the HFD. Consistently, there were significant effects of Vitexin on important regulators of lipid metabolism, including AMP-activated protein kinase-α (AMPKα), CAATT element binding protein-α (C/EBPα), and fatty acid synthase (FAS) in white adipose tissue. Moreover, Vitexin significantly inhibited fat accumulation in 3T3-L1 adipocytes, and this was totally abolished by compound C (an AMPKα inhibitor). These results suggest that Vitexin may prevent HFD-induced obesity/adipogenesis via the AMPKα mediated pathway.
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Vitexin ameliorates high fat diet-induced obesity in male C57BL/6J mice via the AMPKα-mediated pathway
Food & function, 2019Co-Authors: Ye Peng, Quancai Sun, Wengang Jin, Li Yuan, Ruichang GaoAbstract:Vitexin, a bioactive compound isolated from hawthorn leaf extracts, has been reported to exhibit many biological activities, such as anticancer, antioxidation, and adipogenesis inhibition activities. The current study explored the effects of Vitexin on high fat diet (HFD)-induced obesity/adipogenesis in male C57BL/6J mice and 3T3-L1 adipocytes, as well as the underlying mechanisms thereof. Vitexin significantly mitigated HFD-induced body weight gain and adiposity. Vitexin also partially normalized serum, hepatic lipid contents, and decreased adipocyte size induced by the HFD. Consistently, there were significant effects of Vitexin on important regulators of lipid metabolism, including AMP-activated protein kinase-α (AMPKα), CAATT element binding protein-α (C/EBPα), and fatty acid synthase (FAS) in white adipose tissue. Moreover, Vitexin significantly inhibited fat accumulation in 3T3-L1 adipocytes, and this was totally abolished by compound C (an AMPKα inhibitor). These results suggest that Vitexin may prevent HFD-induced obesity/adipogenesis via the AMPKα mediated pathway.
