10 research outputs found

    <i>Cassia tora</i> Seed Extract and Its Active Compound Aurantio-obtusin Inhibit Allergic Responses in IgE-Mediated Mast Cells and Anaphylactic Models

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    <i>Cassia tora</i> seed is widely used due to its various biological properties including anticancer, antidiabetic, and anti-inflammatory effects. However, there has been no report of the effects of <i>C. tora</i> seed extract (CTE) on immunoglobulin E (IgE)-mediated allergic responses. In this research, we demonstrated the effects of CTE and its active compound aurantio-obtusin on IgE-sensitized allergic reactions in mast cells and passive cutaneous anaphylaxis (PCA). CTE and aurantio-obtusin suppressed degranulation, histamine production, and reactive oxygen species generation and inhibited the production and mRNA expression of tumor necrosis factor-α and interleukin-4. CTE and aurantio-obtusin also suppressed the prostaglandin E<sub>2</sub> production and expression of cyclooxygenase 2. Furthermore, CTE and aurantio-obtusin suppressed IgE-mediated FcεRI signaling such as phosphorylation of Syk, protein kinase Cμ, phospholipase Cγ, and extracellular signal-regulated kinases. CTE and aurantio-obtusin blocked mast cell-dependent PCA in IgE-mediated mice. These results suggest that CTE and aurantio-obtusin are a beneficial treatment for allergy-related diseases

    Gomisin J Inhibits Oleic Acid-Induced Hepatic Lipogenesis by Activation of the AMPK-Dependent Pathway and Inhibition of the Hepatokine Fetuin‑A in HepG2 Cells

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    The aim of our study is to investigate the molecular mechanism of gomisin J from Schisandra chinensis on the oleic acid (OA)-induced lipid accumulation in HepG2 cells. Gomisin J attenuated lipid accumulation in OA-induced HepG2 cells. It also suppressed the expression of lipogenic enzymes and inflammatory mediators and increased the expression of lipolytic enzymes in OA-induced HepG2 cells. Furthermore, the use of specific inhibitors and fetuin-A siRNA and liver kinase B1 (LKB1) siRNA transfected cells demonstrated that gomisin J regulated lipogenesis and lipolysis via inhibition of fetuin-A and activation of an AMP-activated protein kinase (AMPK)-dependent pathway in HepG2 cells. Our results showed that gomisin J suppressed lipid accumulation by regulating the expression of lipogenic and lipolytic enzymes and inflammatory molecules through activation of AMPK, LKB1, and Ca<sup>2+</sup>/calmodulin-dependent protein kinase II and inhibition of fetuin-A in HepG2 cells. This suggested that gomisin J has potential benefits in treating nonalcoholic fatty liver disease

    Aceriphyllum rossii Extract and Its Active Compounds, Quercetin and Kaempferol Inhibit IgE-mediated Mast Cell Activation and Passive Cutaneous Anaphylaxis

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    Aceriphyllum rossii contains an abundant source of natural flavonoids with potential antioxidant, anticancer and anti-inflammatory properties. However, the effect of A. rossii extract (ARE) on immunoglobulin E­(IgE)-mediated allergic responses remains unknown. In the present study, the effects of ARE and its active compounds, quercetin and kaempferol, on IgE-mediated rat basophilic leukemia mast cell activation and passive cutaneous anaphylaxis (PCA) were investigated. ARE, quercetin, and kaempferol inhibited secretion of β-hexosaminidase and histamine, and reduced the production and mRNA expression of interleukin-4 and tumor necrosis factor-α. ARE also decreased the production of prostaglandin E<sub>2</sub> and leukotriene B<sub>4</sub> and expression of cyclooxygenase 2 and 5-lipoxygenase. Furthermore, ARE, quercetin, and kaempferol inhibited IgE-mediated phosphorylation of Syk, phospholipase Cγ, protein kinase C (PKC)­μ, and the mitogen-activated protein kinases, extracellular signal-regulated kinase, p38, and c-Jun N-terminal kinase. ARE, quercetin, and kaempferol markedly suppressed mast cell-dependent PCA in IgE-sensitized mice. These results indicate that ARE and its active constituents, quercetin and kaempferol, may be a useful therapy for immediate-type hypersensitivity

    Antimicrobial Air Filters Using Natural <i>Euscaphis japonica</i> Nanoparticles

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    <div><p>Controlling bioaerosols has become more important with increasing participation in indoor activities. Treatments using natural-product nanomaterials are a promising technique because of their relatively low toxicity compared to inorganic nanomaterials such as silver nanoparticles or carbon nanotubes. In this study, antimicrobial filters were fabricated from natural <i>Euscaphis japonica</i> nanoparticles, which were produced by nebulizing <i>E</i>. <i>japonica</i> extract. The coated filters were assessed in terms of pressure drop, antimicrobial activity, filtration efficiency, major chemical components, and cytotoxicity. Pressure drop and antimicrobial activity increased as a function of nanoparticle deposition time (590, 855, and 1150 µg/cm2<sub>filter</sub> at 3-, 6-, and 9-min depositions, respectively). In filter tests, the antimicrobial efficacy was greater against <i>Staphylococcus epidermidis</i> than <i>Micrococcus luteus</i>; ~61, ~73, and ~82% of <i>M</i>. <i>luteus</i> cells were inactivated on filters that had been coated for 3, 6, and 9 min, respectively, while the corresponding values were ~78, ~88, and ~94% with <i>S</i>. <i>epidermidis</i>. Although statistically significant differences in filtration performance were not observed between samples as a function of deposition time, the average filtration efficacy was slightly higher for <i>S</i>. <i>epidermidis</i> aerosols (~97%) than for <i>M</i>. <i>luteus</i> aerosols (~95%). High-performance liquid chromatography (HPLC) and electrospray ionization-tandem mass spectrometry (ESI/MS) analyses confirmed that the major chemical compounds in the <i>E</i>. <i>japonica</i> extract were 1(ß)-<i>O</i>-galloyl pedunculagin, quercetin-3-<i>O</i>-glucuronide, and kaempferol-3-<i>O</i>-glucoside. <i>In vitro</i> cytotoxicity and disk diffusion tests showed that <i>E</i>. <i>japonica</i> nanoparticles were less toxic and exhibited stronger antimicrobial activity toward some bacterial strains than a reference soluble nickel compound, which is classified as a human carcinogen. This study provides valuable information for the development of a bioaerosol control system that is environmental friendly and suitable for use in indoor environments.</p></div

    Secretome Profiling Reveals the Signaling Molecules of Apoptotic HCT116 Cells Induced by the Dietary Polyacetylene Gymnasterkoreayne B

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    Dietary polyacetylenes from various foods have been receiving attention as promising cancer chemopreventive agents. However, until now, the detailed molecular mechanism and the regulatory proteins underlying these effects have not been elucidated. We investigated the effects of gymnasterkoreayne B (GKB), a model dietary polyacetylene from wild vegetables, on the programmed cell death of HCT116 human colorectal cancer cells. GKB inhibited HCT116 cell proliferation by inducing apoptotic cell death. GKB treatment resulted in ROS accumulation, leading to the activation of both intrinsic and extrinsic apoptotic pathway. We also found that FN1, TGFB1, APP, SERPINE1, HSPD1, SOD1, TXN, and ACTN4 may act as secretory signaling molecules during GKB-induced apoptotic cell death using LC–MS/MS identification followed by spectrum counting, statistical calculation, and gene ontology analysis. The secretory proteins suggested in this study may be promising candidates involved in apoptotic cell death of cancer cells induced by GKB that warrant further functional study

    Concentrations, GSD, GMD, and peak diameters of test bacterial bioaerosols (<i>n</i> = 3).

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    <p><sup>1</sup>GSD, geometric standard deviation.</p><p><sup>2</sup>GMD, geometric mean diameter.</p><p>Concentrations, GSD, GMD, and peak diameters of test bacterial bioaerosols (<i>n</i> = 3).</p

    The inhibitory effects of <i>E</i>. <i>japonica</i> and a soluble nickel compound (SNC) on A549 cancer and HEL 299 cells.

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    <p>Error bars indicate standard deviations (<i>n</i> = 10) <sup>1</sup>Half maximal inhibitory concentration, <sup>2</sup>A549 human lung adenocarcinoma cancer cells, <sup>3</sup>HEL 299 human lung fibroblast cells.</p
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