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Astragalin

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Younghee Kang – 1st expert on this subject based on the ideXlab platform

  • Astragalin Inhibits Pulmonary Inflammation in Cigarette Smoking-Induced Embolism
    Current Developments in Nutrition, 2020
    Co-Authors: Younghee Kang

    Abstract:

    Abstract

    Objectives
    Thrombin generation is crucial to the regulation of hemostasis and thrombosis and is essential to the pathogenesis of cardiovascular disease and venous thrombosis. Pulmonary embolism is a blockage in one of the pulmonary arteries in your lung caused by blood clots due to risk factors including tobacco use. Astragalin (kaempferol 3-O-glucoside) is a flavonoid present in persimmon leaves and green tea seeds and exhibits diverse activities such as asthma and obstructive pulmonary disease. This study investigated that Astragalin encumbered pulmonary inflammation caused by cigarette smoking-induced embolism.

    Methods
    Pulmonary embolism was evoked through exposure of BALB/c mice to cigarette smoke for 30 min, five days a week for eight weeks. Mice were orally administrated with 10 or 20 mg/kg Astragalin for 8 weeks. For the in vitro studies, 10 U/ml thrombin was loaded to alveolar epithelial A549 cells in the absence and presence of 1–20 μM Astragalin.

    Results
    Oral supplementation of Astragalin reduced tissue factor and urokinase-type plasminogen activator elevated in cigarette smoking-exposed lungs. In addition, 1–20 μM Astragalin attenuated the induction of protease activated receptor-1 known as coagulation factor II (thrombin) receptor-like-1, in 10 U/ml thrombin-loaded alveolar epithelial cells. Astragalin curtailed induction of the inflammatory mediators of cyclooxygenase-2, intercellular adhesion molecule-1 and inducible nitric oxide synthase in alveolar cells subjected to thrombin. Furthermore, Astragalin inhibited inflammatory signaling entailing MAPK/ERK pathway.

    Conclusions
    Astragalin may be a potential agent alleviating pulmonary inflammation induced by cigarette smoking-induced embolism.

    Funding Sources
    This research was supported by Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Education (2019R1A6A3A01094891).

  • Astragalin inhibits allergic inflammation and airway thickening in ovalbumin challenged mice
    Journal of Agricultural and Food Chemistry, 2017
    Co-Authors: Yeanjung Choi, Minkyung Kang, Sinhye Park, Lucia Dwi Antika, Younghee Kang

    Abstract:

    Lung inflammation and oxidative stress are the major contributors to the development of obstructive pulmonary diseases. Macrophages are involved in pulmonary inflammation and alveolar damage in emphysema. Astragalin is an anti-inflammatory flavonoid present in persimmon leaves and green tea seeds. This study elucidated that Astragalin inhibited inflammatory cell infiltration induced by 20 μM H2O2 and blocked airway thickening and alveolar emphysema induced by 20 μg of ovalbumin (OVA) in mice. OVA induced mouse pulmonary MCP-1, and H2O2 enhanced the expression of MCP-1/ICAM-1/αv integrin in bronchial airway epithelial BEAS-2B cells. Such induction was inhibited by supplying 10–20 mg/kg of Astragalin to OVA-challenged mice and 1–20 μM Astragalin to oxidant-stimulated cells. Oral administration of 20 mg/kg of Astragalin reduced the induction of F4/80/CD68/CD11b in airways of mice challenged with OVA. Additionally, emphysema tissue damage was observed in OVA-exposed alveoli. Mast cell recruitment in the airwa…

  • Astragalin inhibits autophagy associated airway epithelial fibrosis
    Respiratory Research, 2015
    Co-Authors: Yeanjung Choi, Juhyun Gong, Minkyung Kang, Daekeun Shin, Younghee Kang

    Abstract:

    Fibrotic remodeling of airway and lung parenchymal compartments is attributed to pulmonary dysfunction with an involvement of reactive oxygen species (ROS) in chronic lung diseases such as idiopathic pulmonary fibrosis and asthma. The in vitro study elucidated inhibitory effects of Astragalin, kaempferol-3-O-glucoside from leaves of persimmon and green tea seeds, on oxidative stress-induced airway fibrosis. The in vivo study explored the demoting effects of Astragalin on epithelial to mesenchymal transition in BALB/c mice sensitized with ovalbumin (OVA). The exposure of 20 μM H2O2 for 72 h accelerated E-cadherin loss and vimentin induction in airway epithelial BEAS-2B cells, which was reversed by non-toxic Astragalin at 1–20 μM. Astragalin allayed the airway tissue levels of ROS and vimentin enhanced by OVA challenge. Collagen type 1 production increased in H2O2–exposed epithelial cells and collagen fiber deposition was observed in OVA-challenged mouse airways. This study further investigated that the oxidative stress-triggered autophagic regulation was responsible for inducing airway fibrosis. H2O2 highly enhanced the expression induction of the autophagy-related beclin-1 and light chains 3A/B (LC3A/B) within 4 h and Astragalin blocked such induction by H2O2. This compound deterred the ROS-promoted autophagosome formation in BEAS-2B cells. Consistently, in OVA-sensitized mice the expression of beclin-1 and LC3A/B was highly induced, and oral administration of Astragalin suppressed the autophagosome formation with inhibiting the induction of these proteins in OVA-challenged airway subepithelium. Induction of autophagy by spermidine influenced the epithelial induction of E-cadherin and vimentin that was blocked by treating Astragalin. These results demonstrate that Astragalin can be effective in allaying ROS-promoted bronchial fibrosis through inhibiting autophagosome formation in airways.

Jae Hyoung Jeon – 2nd expert on this subject based on the ideXlab platform

  • hydrophilic Astragalin galactoside induces t helper type 1 mediated immune responses via dendritic cells
    International Journal of Molecular Sciences, 2018
    Co-Authors: Jae Hyoung Jeon

    Abstract:

    A flavonoid Astragalin (kaempferol-3-O-β-d-glucopyranoside, Ast) has several biological activities including anti-oxidant, anti-HIV, and anti-allergic effects. Nonetheless, its insolubility in hydrophilic solvents imposes restrictions on its therapeutic applications. In this study, we investigated the effects of water-soluble Astragalin-galactoside (kaempferol-3-O-β-d-isomaltotrioside, Ast-Gal) on murine bone marrow-derived dendritic cell (DC) maturation and T helper (Th) cell-mediated immune responses. Ast-Gal significantly increased maturation and activation of DCs through the upregulation of surface markers, such as cluster of differentiation (CD)80, CD86, and Major histocompatibility complex (MHC) II in a dose-dependent manner, while Ast had little effects. Additionally, Ast-Gal-treated DCs markedly secreted immune-stimulating cytokines such as interleukin (IL)-1β, IL-6, and IL-12. Importantly, Ast-Gal strongly increased expression of IL-12, a polarizing cytokine of Th1 cells. In a co-culture system of DCs and CD4+ T cells, Ast-Gal-treated DCs preferentially differentiates naive CD4+ T cells into Th1 cells. The addition of neutralizing IL-12 monoclonal antibody (mAb) to cultures of Ast-Gal-treated DCs and CD4+ T cells significantly decreased interferon (IFN)-γ production, thereby indicating that Ast-Gal-stimulated DCs enhance the Th1 response through IL-12 production by DCs. Injection with Ast-Gal-treated DCs in mice increased IFN-γ-secreting Th1 cell population. Collectively, these findings indicate that hydrophilically modified Astragalin can enhance Th1-mediated immune responses via DCs and point to a possible application of water-soluble Astragalin-galactoside as an immune adjuvant.

  • Hydrophilic Astragalin Galactoside Induces T Helper Type 1-Mediated Immune Responses via Dendritic Cells
    , 2018
    Co-Authors: Jae Hyoung Jeon

    Abstract:

    A flavonoid Astragalin (kaempferol-3-O-β-D-glucopyranoside, Ast) has several biological activities including anti-oxidant, anti-HIV, and anti-allergic effects. Nonetheless, its insolubility in hydrophilic solvents imposes restrictions on its therapeutic applications. In this study, we investigated the effects of water-soluble Astragalin-galactoside (kaempferol-3-O- β-D-isomaltotrioside, Ast-Gal) on dendritic cell (DC) maturation and T helper (Th) cell-mediated immune responses. Ast-Gal significantly increased maturation and activation of DCs through up-regulation of surface markers, such as CD80, CD86, and MHC II in a dose-dependent manner, while Ast had little effects. Also, Ast-Gal-treated DCs markedly secreted immune-stimulating cytokines such as IL-1β, IL-6, and IL-12. Importantly, Ast-Gal strongly increased expression of IL-12, a polarizing cytokine of Th1 cells. In a co-culture system of DCs and CD4+ T cells, Ast-Gal-treated DCs preferentially differentiates naïve CD4+ T cells into Th1 cells. The addition of neutralizing IL-12 mAb to cultures of Ast-Gal-treated DCs and CD4+ T cells significantly increased IFN- γ production, thereby indicating that Ast-Gal-stimulated DCs enhance the Th1 response through IL-12 production by DCs. Injection with Ast-Gal-treated DCs in mice increased IFN-γ-secreting Th1 cell population. Collectively, these findings indicate that hydrophilically modified Astragalin can enhance Th1-mediated immune responses via DCs, and point to a possible application of water-soluble Astragalin-galactoside as an immune adjuvant.

Dong Wang – 3rd expert on this subject based on the ideXlab platform

  • Astragalin and dihydromyricetin as adjuncts to histidine tryptophan ketoglutarate cardioplegia enhances protection during cardioplegic arrest
    Molecular Medicine Reports, 2018
    Co-Authors: Dong Wang, Daoxu Qu, Xinjie Zhang, Fanqing Meng, Minglei Xu, Qiusheng Zheng

    Abstract:

    : The present study used an in vitro model of cold cardioplegia in isolated working rat hearts to evaluate the possible effects of two flavonoids, Astragalin and dihydromyricetin, as adjuncts to histidine‑tryptophan‑ketoglutarate (HTK) cardioplegia. The following three groups of male Sprague Dawley rats were evaluated: The HTK group, treated with HTK alone; the HTK‑A group, treated with 10 µmol/l Astragalin; and the HTK‑D group, treated with 10 µmol/l dihydromyricetin. Isolated rat hearts were perfused with Krebs‑Henseleit buffer for 30 min and incubated with the respective cardioplegic solution for 6 h at 4˚C. Subsequently, Astragalin or dihydromyricetin was added to the cardioplegic solutions. Following 30 min of reperfusion, the left ventricular developed pressure (LVDP), maximum up/down rate of left ventricular pressure (±dp/dtmax) and heart rate were documented as indices of myocardial function using a physiological recorder. Myocardial infarct size (IS) was estimated using 2,3,5‑triphenyltetrazolium chloride staining. Lactate dehydrogenase (LDH) and creatine kinase (CK) levels were also determined to assess the degree of cardiac injury. Cardiomyocyte apoptosis analysis was performed using an in situ cell death detection kit. In addition, malondialdehyde (MDA), superoxide dismutase (SOD), interleukin‑6 (IL‑6), tumor necrosis factor‑α (TNF‑α), C‑reactive protein (CRP) levels, as well as the glutathione/glutathione disulfide (GSH/GSSG) ratio were determined and analyzed using ELISA kits. The protein levels of caspase‑9 and B‑cell lymphoma‑2 (Bcl‑2) were determined using western blot analysis. The results demonstrated that exposure to Astragalin or dihydromyricetin significantly improved the recovery of LVDP (P<0.05 and P<0.01, respectively), the +dP/dtmax (P<0.05 for dihydromyricetin only) and the ‑dP/dtmax (P<0.05 and P<0.01, respectively), increased SOD levels (P<0.05 and P<0.01, respectively) and GSH/GSSG ratios (P<0.05), reduced myocardial IS (P<0.05 and P<0.01, respectively), decreased CK, LDH, IL‑6 (all P<0.05 and P<0.01, respectively), MDA (P<0.05), CRP (P<0.05) and TNF‑α levels (P<0.05 and P<0.01, respectively), increased Bcl‑2 levels (P<0.01) and decreased caspase‑9 levels (P<0.01). The results indicated that the addition of either flavonoid (particularly dihydromyricetin) to HTK enhances protection during ischemia, decreases myocardial dysfunction by enhancing anti‑inflammatory activities, attenuates myocardial oxidative injury and prevents apoptosis during ischemia/reperfusion.

  • Astragalin and dihydromyricetin as adjuncts to histidine‑tryptophan‑ketoglutarate cardioplegia enhances protection during cardioplegic arrest
    Molecular Medicine Reports, 2018
    Co-Authors: Dong Wang, Daoxu Qu, Xinjie Zhang, Fanqing Meng, Minglei Xu, Qiusheng Zheng

    Abstract:

    : The present study used an in vitro model of cold cardioplegia in isolated working rat hearts to evaluate the possible effects of two flavonoids, Astragalin and dihydromyricetin, as adjuncts to histidine‑tryptophan‑ketoglutarate (HTK) cardioplegia. The following three groups of male Sprague Dawley rats were evaluated: The HTK group, treated with HTK alone; the HTK‑A group, treated with 10 µmol/l Astragalin; and the HTK‑D group, treated with 10 µmol/l dihydromyricetin. Isolated rat hearts were perfused with Krebs‑Henseleit buffer for 30 min and incubated with the respective cardioplegic solution for 6 h at 4˚C. Subsequently, Astragalin or dihydromyricetin was added to the cardioplegic solutions. Following 30 min of reperfusion, the left ventricular developed pressure (LVDP), maximum up/down rate of left ventricular pressure (±dp/dtmax) and heart rate were documented as indices of myocardial function using a physiological recorder. Myocardial infarct size (IS) was estimated using 2,3,5‑triphenyltetrazolium chloride staining. Lactate dehydrogenase (LDH) and creatine kinase (CK) levels were also determined to assess the degree of cardiac injury. Cardiomyocyte apoptosis analysis was performed using an in situ cell death detection kit. In addition, malondialdehyde (MDA), superoxide dismutase (SOD), interleukin‑6 (IL‑6), tumor necrosis factor‑α (TNF‑α), C‑reactive protein (CRP) levels, as well as the glutathione/glutathione disulfide (GSH/GSSG) ratio were determined and analyzed using ELISA kits. The protein levels of caspase‑9 and B‑cell lymphoma‑2 (Bcl‑2) were determined using western blot analysis. The results demonstrated that exposure to Astragalin or dihydromyricetin significantly improved the recovery of LVDP (P

  • cardioprotective effects of Astragalin against myocardial ischemia reperfusion injury in isolated rat heart
    Oxidative Medicine and Cellular Longevity, 2016
    Co-Authors: Daoxu Qu, Wenxiao Yang, Xinjie Zhang, Qiusheng Zheng, Dong Wang

    Abstract:

    This study aims to evaluate the cardioprotective effects of Astragalin against myocardial ischemia/reperfusion (I/R) injury in isolated rat heart. The cardioprotective effects of Astragalin on myocardial I/R injury were investigated on Langendorff apparatus. Adult male Sprague-Dawley rats were randomly divided into five groups. The results showed that Astragalin pretreatment improved myocardial function. Compared with I/R group, lactate dehydrogenase (LDH) and creatine kinase (CK) activities in coronary flow decreased in Astragalin pretreatment groups, whereas superoxide dismutase (SOD) activity and glutathione/glutathione disulfide (GSH/GSSG) ratio significantly increased. The levels of malondialdehyde (MDA), intracellular reactive oxygen species (ROS), tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6) decreased in Astragalin-treated groups. The infarct size (IS) and apoptosis rate in hearts from Astragalin-treated groups were lower than those in hearts from the I/R group. Western blot analysis also revealed that Astragalin preconditioning significantly reduced Bax level, whereas Bcl-2 was increased in the myocardium. Therefore, Astragalin exhibited cardioprotective effects via its antioxidative, antiapoptotic, and anti-inflammatory activities.