Astragalin

1 Aesculus sp. 2 Allium sp. 3 Alkanna sp. 4 Arctium sp. 5 Asplenium sp. 6 Castanea sp. 7 Cichorium sp. 8 Cornus sp. 9 Cucurbita sp. 10 Cyamopsis sp. 11 Dionaea sp. 12 Equisetum sp. 13 Eriodictyon sp. 14 Eryngium sp. 15 Euphorbia sp. 16 Geranium sp. 17 Ginkgo sp. 18 Glycyrrhiza sp. 19 Gossypium sp. 20 Hamamelis sp. 21 Humulus sp. 22 Illicium sp. 23 Lamium sp. 24 Larix sp. 25 Laurus sp. 26 Liquidambar sp. 27 Liriodendron sp. 28 Menyanthes sp. 29 Oenothera sp. 30 Orchis sp. 31 Paeonia sp. 32 Phyllanthus sp. 33 Phytolacca sp. 34 Platanus sp. 35 Primula sp. 36 Rhamnus sp. 37 Ribes sp. 38 Rosa sp. 39 Sambucus sp. 40 Sanguisorba sp. 41 Senecio sp. 42 Serenoa sp. 43 Solidago sp. 44 Syzygium sp. 45 Tilia sp. 46 Trigonella sp. 47 Urtica sp. 48 Viburnum sp.

Astragalin (kaempferol-3-O-glucoside) is a flavonoid with anti-inflammatory activity and newly found in persimmon leaves and green tea seeds. IC50 value: Target: in vitro: Astragalin nontoxic at ≤ 20 μM suppressed cellular induction of Toll-like receptor 4 (TLR4) and ROS production enhanced by LPS. Both LPS and H2O2 induced epithelial eotaxin-1 expression, which was blocked by astragalin. LPS activated and induced PLCγ1, PKCβ2, and NADPH oxidase subunits of p22phox and p47phox in epithelial cells and such activation and induction were demoted by astragalin or TLR4 inhibition antagonizing eotaxin-1 induction. H2O2-upregulated phosphorylation of JNK and p38 MAPK was dampened by adding astragalin to epithelial cells, while this compound enhanced epithelial activation of Akt and ERK. H2O2 and LPS promoted epithelial apoptosis concomitant with nuclear condensation or caspase-3 activation, which was blunted by astragalin [1]. astragalin suppressed the expression of tumor necrosis factor α, interleukin 6, and nitric oxide in a dose-dependent manner in mMECs [2]. astragalin attenuated the infiltration of inflammatory cells, the activity of myeloperoxidase (MPO) and the expression of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and interleukin-1β (IL-1β) in a dose-dependent manner. Additionally, Western blotting results showed that astragalin efficiently blunt decreased nuclear factor-kappaB (NF-κB) activation by inhibiting the degradation and phosphorylation of IκBα and the nuclear translocation of p65 [3]. Astragalin significantly reduced LPS-induced expression of iNOS, COX-2 and cytokines/chemokines, and production of NO in J774A.1 mouse macrophages. Astragalin inhibited LPSinduced activation of NF-κB as indicated by inhibition of degradation of IκBα, nuclear translocation of NF-κB, and NF-κB dependent gene reporter assay [4]. in vivo: Mice were injected intraperitoneally (i.p.) with lipopolysaccharide (LPS) (dose range: 5-40 mg/kg). pretreatment with astragalin can improve survival during lethal endotoxemia and attenuate inflammatory responses in a murine model of lipopolysaccharide-induced acute lung injury [4].

References:
[1]. Cho IH, et al. Astragalin inhibits airway eotaxin-1 induction and epithelial apoptosis through modulating oxidative stress-responsive MAPK signaling. BMC Pulm Med. 2014 Jul 29;14:122. [2]. Li F, et al. Inhibitory effects of astragalin on lipopolysaccharide-induced inflammatory response in mouse mammary epithelial cells. J Surg Res. 2014 Dec;192(2):573-81. [3]. Li F, et al. Astragalin suppresses inflammatory responses via down-regulation of NF-κB signaling pathway in lipopolysaccharide-induced mastitis in a murine model. Int Immunopharmacol. 2013 Oct;17(2):478-82. [4]. Kim MS, et al. Inhibitory effect of astragalin on expression of lipopolysaccharide-induced inflammatory mediators through NF-κB in macrophages. Arch Pharm Res. 2011 Dec;34(12):2101-7. [5]. Soromou LW, et al. Astragalin attenuates lipopolysaccharide-induced inflammatory responses by down-regulating NF-κB signaling pathway. Biochem Biophys Res Commun. 2012 Mar 9;419(2):256-61.

Astragalin inhibits IL-1beta-induced inflammatory mediators production in human osteoarthritis chondrocyte by inhibiting NF-kappaB and MAPK activation.[Pubmed:25637445]

Int Immunopharmacol. 2015 Mar;25(1):83-7.

Astragalin, a bioactive component isolated from Rosa agrestis, has been described to exhibit anti-inflammatory activity. The aim of this study was to investigate the anti-inflammatory effects and the underlying mechanisms of Astragalin on IL-1beta-stimulated human osteoarthritis chondrocyte. The production of NO and PGE2 was detected by Griess reaction and ELISA. The expression of iNOS and COX-2 was detected by western blotting. The expression of NF-kappaB and MAPKs was detected by western blot analysis. We found that Astragalin dose-dependently inhibited IL-1beta-induced NO and PGE2 production, as well as iNOS and COX-2 expression. Meanwhile, western blot analysis showed that Astragalin inhibited IL-1beta-induced NF-kappaB and MAPK activation in human osteoarthritis chondrocyte. In addition, Astragalin was found to activate PPAR-gamma. The inhibition of Astragalin on IL-1beta-induced NO and PGE2 production can be reversed by PPAR-gamma antagonist GW9662. Astragalin suppressed IL-1beta-induced inflammatory mediators via activating PPAR-gamma, which subsequently inhibited IL-1beta-induced NF-kappaB and MAPK activation. Astragalin may be a potential agent in the treatment of osteoarthritis.

Inhibitory effects of astragalin on lipopolysaccharide-induced inflammatory response in mouse mammary epithelial cells.[Pubmed:24972733]

J Surg Res. 2014 Dec;192(2):573-81.

BACKGROUND: Tea brewed from the leaves of persimmon or Rosa agrestis have several medical functions including treating allergy, antiatopic dermatitis, and anti-inflammatory effects. The objective of this study was to investigate the molecular mechanisms of Astragalin, a main flavonoid component isolated from these herbs, in modifying lipopolysaccharide (LPS)-induced signaling pathways in primary cultured mouse mammary epithelial cells (mMECs). MATERIALS AND METHODS: The mMECs were treated with LPS in the absence or presence of different concentrations of Astragalin. The expression of proinflammatory cytokines tumor necrosis factor alpha, and interleukin 6, as well as nitric oxide production were determined by enzyme-linked immunosorbent assay and Griess reaction, respectively. Cyclooxygenase-2, inducible nitric oxide synthase, toll-like receptor 4 (TLR4), nuclear factor-kappaB (NF-kappaB), inhibitor protein of NF-kappaB (IkappaBalpha), P38, extracellular signal-regulated kinase, and c-Jun N-terminal kinase were measured by Western blot. RESULTS: The results showed that Astragalin suppressed the expression of tumor necrosis factor alpha, interleukin 6, and nitric oxide in a dose-dependent manner in mMECs. Western blot results showed that the expression of inducible nitric oxide synthase and cyclooxygenase-2 was inhibited by Astragalin. Besides, Astragalin efficiently decreased LPS-induced TLR4 expression, NF-kappaB activation, IkappaBalpha degradation, and the phosphorylation of p38, extracellular signal-regulated kinase in BMECs. CONCLUSIONS: Our results indicated that Astragalin exerts anti-inflammatory properties possibly via the inactivation of TLR4-mediated NF-kappaB and mitogen-activated protein kinases signaling pathways in LPS-stimulated mMECs. Thus, Astragalin may be a potential therapeutic agent for bovine mastitis.

Astragalin suppresses inflammatory responses via down-regulation of NF-kappaB signaling pathway in lipopolysaccharide-induced mastitis in a murine model.[Pubmed:23928506]

Int Immunopharmacol. 2013 Oct;17(2):478-82.

Mastitis is a prevalent and economic disease around the world and defined as infection and inflammation of the mammary gland. Astragalin, a bioactive component isolated from persimmon or Rosa agrestis, has been reported to have anti-inflammatory properties. To investigate the potential therapeutic effect of Astragalin in mastitis, a murine model of mastitis was induced by administration of LPS in mammary gland. Astragalin was applied 1h before and 12h after LPS treatment. The results showed that Astragalin attenuated the infiltration of inflammatory cells, the activity of myeloperoxidase (MPO) and the expression of tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6) and interleukin-1beta (IL-1beta) in a dose-dependent manner. Additionally, Western blotting results showed that Astragalin efficiently blunt decreased nuclear factor-kappaB (NF-kappaB) activation by inhibiting the degradation and phosphorylation of IkappaBalpha and the nuclear translocation of p65. These results suggested that Astragalin exerts anti-inflammatory properties in LPS-mediated mastitis, possibly through inhibiting inhibition of the NF-kappaB signaling pathway, which mediates the expression of pro-inflammatory cytokines. Astragalin may be a potential therapeutic agent against mastitis.

Astragalin inhibits airway eotaxin-1 induction and epithelial apoptosis through modulating oxidative stress-responsive MAPK signaling.[Pubmed:25069610]

BMC Pulm Med. 2014 Jul 29;14:122.

BACKGROUND: Eotaxin proteins are a potential therapeutic target in treating the peribronchial eosinophilia associated with allergic airway diseases. Since inflammation is often associated with an increased generation of reactive oxygen species (ROS), oxidative stress is a mechanistically imperative factor in asthma. Astragalin (kaempferol-3-O-glucoside) is a flavonoid with anti-inflammatory activity and newly found in persimmon leaves and green tea seeds. This study elucidated that Astragalin inhibited endotoxin-induced oxidative stress leading to eosinophilia and epithelial apoptosis in airways. METHODS: Airway epithelial BEAS-2B cells were exposed to lipopolysaccharide (LPS) in the absence and presence of 1-20 muM Astragalin. Western blot and immunocytochemical analyses were conducted to determine induction of target proteins. Cell and nuclear staining was also performed for ROS production and epithelial apoptosis. RESULTS: When airway epithelial cells were exposed to 2 mug/ml LPS, Astragalin nontoxic at Astragalin. LPS activated and induced PLCgamma1, PKCbeta2, and NADPH oxidase subunits of p22phox and p47phox in epithelial cells and such activation and induction were demoted by Astragalin or TLR4 inhibition antagonizing eotaxin-1 induction. H2O2-upregulated phosphorylation of JNK and p38 MAPK was dampened by adding Astragalin to epithelial cells, while this compound enhanced epithelial activation of Akt and ERK. H2O2 and LPS promoted epithelial apoptosis concomitant with nuclear condensation or caspase-3 activation, which was blunted by Astragalin. CONCLUSIONS: Astragalin ameliorated oxidative stress-associated epithelial eosinophilia and apoptosis through disturbing TLR4-PKCbeta2-NADPH oxidase-responsive signaling. Therefore, Astragalin may be a potent agent antagonizing endotoxin-induced oxidative stress leading to airway dysfunction and inflammation.

Astragalin inhibits autophagy-associated airway epithelial fibrosis.[Pubmed:25895672]

Respir Res. 2015 Apr 21;16:51.

BACKGROUND: 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. METHODS: 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). RESULTS: The exposure of 20 muM 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 muM. 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. CONCLUSION: These results demonstrate that Astragalin can be effective in allaying ROS-promoted bronchial fibrosis through inhibiting autophagosome formation in airways.

Astragalin (kaempferol-3-O-glucoside) is a flavonoid with anti-inflammatory activity and newly found in persimmon leaves and green tea seeds.

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