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1.
Phys Chem Chem Phys ; 22(3): 981-984, 2020 Jan 21.
Artigo em Inglês | MEDLINE | ID: mdl-31912822

RESUMO

Herein, we propose a new approach of molecule occupancy via a vapor treatment to facilitate the conversion of PbI2 to perovskite in sequential deposition. We have shown that the morphology of PbI2 and the subsequent crystallization of perovskite can be effectively tuned, thus leading to the elimination of residual PbI2 and promotion of perovskite growth.

2.
Front Pharmacol ; 9: 386, 2018.
Artigo em Inglês | MEDLINE | ID: mdl-29731715

RESUMO

Lipoteichoic acid (LTA) induces neuroinflammatory molecules, contributing to the pathogenesis of neurodegenerative diseases. Therefore, suppression of neuroinflammatory molecules could be developed as a therapeutic method. Although previous data supports an immune-modulating effect of curcumin, the underlying signaling pathways are largely unidentified. Here, we investigated curcumin's anti-neuroinflammatory properties in LTA-stimulated BV-2 microglial cells. Inflammatory cytokine tumor necrosis factor-α [TNF-α, prostaglandin E2 (PGE2), and Nitric Oxide (NO] secretion in LTA-induced microglial cells were inhibited by curcumin. Curcumin also inhibited LTA-induced inducible NO synthases (iNOS) and cyclooxygenase-2 (COX-2) expression. Subsequently, our mechanistic studies revealed that curcumin inhibited LTA-induced phosphorylation of mitogen-activated protein kinase (MAPK) including ERK, p38, Akt and translocation of NF-κB. Furthermore, curcumin induced hemeoxygenase (HO)-1HO-1 and nuclear factor erythroid 2-related factor 2 (Nrf-2) expression in microglial cells. Inhibition of HO-1 reversed the inhibition effect of HO-1 on inflammatory mediators release in LTA-stimulated microglial cells. Taken together, our results suggest that curcumin could be a potential therapeutic agent for the treatment of neurodegenerative disorders via suppressing neuroinflammatory responses.

3.
Food Chem ; 256: 427-434, 2018 Aug 01.
Artigo em Inglês | MEDLINE | ID: mdl-29606470

RESUMO

To help produce hypoallergenic food, this study investigated reducing the allergenicity and improving the functional properties of bovine ß-lactoglobulin (ßLG) by covalent conjugation with (-)-epigallo-catechin 3-gallate (EGCG) and chlorogenic acid (CA). The covalent bond between the polyphenols and the amino acid side-chains in ßLG was confirmed by MALDI-TOF-MS and SDS-PAGE. Structural analysis by fluorescence spectroscopy, circular dichroism (CD) and Fourier transform infrared (FTIR) indicated that the covalent conjugate of EGCG and CA led to the changed protein structure of ßLG. Western blot analysis and enzyme-linked immunosorbent assay indicated that conjugation of ßLG with these polyphenols was effective in reducing the IgE-binding capacity of ßLG. The conjugates maintained the retinol-binding activity without denaturation the protein and enhanced the thermal stability with high antioxidant activity. The study provides an innovative approach to producing hypoallergenic food.


Assuntos
Alérgenos/química , Lactoglobulinas/química , Polifenóis/química , Alérgenos/imunologia , Animais , Catequina/análogos & derivados , Catequina/química , Bovinos , Ácido Clorogênico/química , Dicroísmo Circular , Eletroforese em Gel de Poliacrilamida , Lactoglobulinas/imunologia , Espectrometria de Fluorescência
4.
Int J Mol Med ; 41(1): 521-530, 2018 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-29115589

RESUMO

Curcumin is the main curcuminoid present in Curcuma longa and it has been previously reported to exhibit a wide range of pharmacological activities. In the present study, the inhibitory effects of curcumin on the inflammatory mediators released by Pam3CSK4-stimulated BV-2 microglial cells were investigated. The production of pro-inflammatory mediators and cytokines, including tumor necrosis factor-α (TNF-α) and prostaglandin E2 (PGE2), were measured by enzyme­linked immunosorbent assay (ELISA). The expression of inflammatory genes, including inducible nitric oxide synthase and cyclooxygenase-2, were further investigated using reverse transcription-quantitative polymerase chain reaction. The effects of curcumin on heme oxygenase-1 (HO-1), nuclear factor (erythroid-derived 2)-like 2 (Nrf2), mitogen-activated protein kinase (MAPK) and nuclear factor-κB (NF-κB) signaling pathways were analyzed by western blotting. The results revealed that curcumin dose-dependently inhibited Pam3CSK4-induced nitric oxide, PGE2, and TNF-α secretion. Curcumin suppressed the secretion of inflammatory mediators through an increase in the expression of HO-1. Curcumin induced HO-1 transcription and translation through the Nrf2/antioxidant response element signaling pathway. Inhibitory experiments revealed that HO-1 was required for the anti-inflammatory effects of curcumin. Further mechanistic studies demonstrated that curcumin inhibited neuroinflammation by suppressing NF-κB and MAPK signaling pathways in Pam3CSK4-activated microglial cells. The results of the present study suggest that curcumin may be a novel treatment for neuroinflammation-mediated neurodegenerative disorders.


Assuntos
Curcumina/administração & dosagem , Inflamação/tratamento farmacológico , Lipopeptídeos/genética , Doenças Neurodegenerativas/tratamento farmacológico , Elementos de Resposta Antioxidante/genética , Linhagem Celular , Dinoprostona/genética , Regulação da Expressão Gênica/efeitos dos fármacos , Heme Oxigenase-1/antagonistas & inibidores , Heme Oxigenase-1/genética , Humanos , Inflamação/genética , Inflamação/patologia , Lipopeptídeos/administração & dosagem , MAP Quinase Quinase 1/antagonistas & inibidores , MAP Quinase Quinase 1/genética , Microglia/efeitos dos fármacos , Microglia/patologia , Fator 2 Relacionado a NF-E2/antagonistas & inibidores , Fator 2 Relacionado a NF-E2/genética , Doenças Neurodegenerativas/genética , Doenças Neurodegenerativas/patologia , Óxido Nítrico/genética , Transdução de Sinais/efeitos dos fármacos , Fator de Necrose Tumoral alfa/genética
5.
Angew Chem Int Ed Engl ; 56(43): 13470-13474, 2017 10 16.
Artigo em Inglês | MEDLINE | ID: mdl-28834589

RESUMO

The regioselective transformation of heterobuckybowl trichalcogenasumanenes 1 a,b at peripheral butoxy groups afforded trichalcogenasumanene ortho-quinones 2 a,b. Compounds 2 a,b are distinct from 1 a,b in terms of their molecular geometry and electronic state; that is, they have a shallower bowl depth and show absorbance in the NIR region. The reaction of 2 a,b with diamines resulted in a variety of heteropolycycles, including molecular spoon 3 a-6 a, planar π-systems 3 b-6 b, and highly twisted [7-6-6]-fused systems 7 a,b. These new heteropolycycles had different optical/electrical properties: 4 a,b showed hole mobility of approximately 0.002 cm2 V-1 s-1 , 6 a displayed red emission in both solution and the solid state, and 7 a,b formed tight stacks of the curved π-surface.

6.
J Med Food ; 20(6): 577-585, 2017 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-28486011

RESUMO

Acteoside, the predominant polyphenol of small-leaved kudingcha, the Chinese tea, has various biological activities. In this study, we examined the acyl migration of acteoside to isoacteoside with high-temperature treatment of acteoside. The inhibitory effects of acyl-migrated acteoside and acteoside on α-amylase were investigated, as were their binding interaction with α-amylase. The binding of acteoside and isoacteoside to α-amylase was investigated by using the fluorescence spectra assay, circular dichroism, and protein-ligand docking studies. Acteoside was more effective than preheated acteoside and isoacteoside in inhibiting α-amylase activity. Acteoside and isoacteoside binding to α-amylase may induce conformational changes to α-amylase, and the binding site of acteoside and isoacteoside being near the active site pocket of α-amylase may explain the decreased activity of α-amylase. The different affinities and binding sites of acteoside and isoacteoside for α-amylase resulted in different inhibition rates, which may be due to structural differences between acteoside and isoacteoside.


Assuntos
Inibidores Enzimáticos/química , Glucosídeos/química , Ligustrum/química , Fenóis/química , alfa-Amilases/antagonistas & inibidores , Cinética , Folhas de Planta/química , Preparações de Plantas , Chá/química , alfa-Amilases/química
7.
Integr Biol (Camb) ; 8(9): 968-75, 2016 09 12.
Artigo em Inglês | MEDLINE | ID: mdl-27515449

RESUMO

Toll-like receptors (TLRs) expressed on mast cells are essential for effective host defense against a wide variety of pathogens. Previous studies have demonstrated that both TLR2 agonists Pam3CSK4 and PGN stimulated IL-8 release in human mast cells. To determine the molecular basis for this phenomenon, we utilized human mast cell line LAD2 cells. We found that only the release of IL-8 stimulated by Pam3CSK4 was TLR2-mediated, which was confirmed by specific TLR2 shRNA. Heterotrimeric G proteins have been previously implicated in TLR signaling in macrophages and monocytes. In the current study, we showed that PamCSK4 induced the activation of MAPKs, NF-κB, PI3K-Akt and Ca(2+)-calcineurin-NFAT signaling cascades in LAD2 cells. Go proteins were required for the activation of MAPKs and NF-κB in TLR2 stimulated LAD2 cells. Therefore, the genetic depletion of Gαo proteins also led to the reduction of the release of IL-8 in LAD2 cells. Taken together, the data presented here suggest that TLR2 activation in human mast cells promotes the release of inflammatory mediators via distinct signaling pathways that partially depend on the action of Go proteins.


Assuntos
Subunidades alfa Gi-Go de Proteínas de Ligação ao GTP/metabolismo , Mediadores da Inflamação/metabolismo , Interleucina-8/metabolismo , Mastócitos/metabolismo , Quinases de Proteína Quinase Ativadas por Mitógeno/metabolismo , NF-kappa B/metabolismo , Receptor 2 Toll-Like/metabolismo , Linhagem Celular , Células Cultivadas , Regulação da Expressão Gênica/fisiologia , Humanos , Transdução de Sinais/fisiologia
8.
Science ; 338(6112): 1344-8, 2012 Dec 07.
Artigo em Inglês | MEDLINE | ID: mdl-23224554

RESUMO

Mechanisms of DNA repair and mutagenesis are defined on the basis of relatively few proteins acting on DNA, yet the identities and functions of all proteins required are unknown. Here, we identify the network that underlies mutagenic repair of DNA breaks in stressed Escherichia coli and define functions for much of it. Using a comprehensive screen, we identified a network of ≥93 genes that function in mutation. Most operate upstream of activation of three required stress responses (RpoS, RpoE, and SOS, key network hubs), apparently sensing stress. The results reveal how a network integrates mutagenic repair into the biology of the cell, show specific pathways of environmental sensing, demonstrate the centrality of stress responses, and imply that these responses are attractive as potential drug targets for blocking the evolution of pathogens.


Assuntos
Quebras de DNA de Cadeia Dupla , Reparo do DNA/genética , Escherichia coli/genética , Regulação Bacteriana da Expressão Gênica , Redes Reguladoras de Genes , Estresse Fisiológico/genética , Proteínas de Bactérias/genética , Mutagênese/genética , Fator sigma/genética
9.
PLoS Genet ; 7(8): e1002223, 2011 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-21901104

RESUMO

Copy-number variations (CNVs) constitute very common differences between individual humans and possibly all genomes and may therefore be important fuel for evolution, yet how they form remains elusive. In starving Escherichia coli, gene amplification is induced by stress, controlled by the general stress response. Amplification has been detected only encompassing genes that confer a growth advantage when amplified. We studied the structure of stress-induced gene amplification in starving cells in the Lac assay in Escherichia coli by array comparative genomic hybridization (aCGH), with polymerase chain reaction (pcr) and DNA sequencing to establish the structures generated. About 10% of 300 amplified isolates carried other chromosomal structural change in addition to amplification. Most of these were inversions and duplications associated with the amplification event. This complexity supports a mechanism similar to that seen in human non-recurrent copy number variants. We interpret these complex events in terms of repeated template switching during DNA replication. Importantly, we found a significant occurrence (6 out of 300) of chromosomal structural changes that were apparently not involved in the amplification event. These secondary changes were absent from 240 samples derived from starved cells not carrying amplification, suggesting that amplification happens in a differentiated subpopulation of stressed cells licensed for global chromosomal structural change and genomic instability. These data imply that chromosomal structural changes occur in bursts or showers of instability that may have the potential to drive rapid evolution.


Assuntos
Instabilidade Cromossômica , Cromossomos Bacterianos/química , Variações do Número de Cópias de DNA/genética , Escherichia coli/genética , Escherichia coli/fisiologia , Amplificação de Genes/genética , Inversão Cromossômica/genética , Hibridização Genômica Comparativa , Evolução Molecular , Duplicação Gênica , Óperon Lac/genética , Estresse Fisiológico
10.
J Biol Chem ; 285(45): 35047-55, 2010 Nov 05.
Artigo em Inglês | MEDLINE | ID: mdl-20801882

RESUMO

Mucus-secreting cells of the stomach epithelium provide a protective barrier against damage that might result from bacterial colonization or other stimuli. Impaired barrier function contributes to chronic inflammation and cancer. Knock-out mice for the epithelium-specific transcription factor Spdef (also called Pdef) have defects in terminal differentiation of intestinal and bronchial secretory cells. We sought to determine the physiologic function of Spdef in the stomach, another site of significant levels of Spdef expression. We used in situ hybridization and immunohistochemistry to localize Spdef-expressing cells in the mouse stomach; targeted gene disruption to generate mice lacking Spdef; and histologic, immunologic, and transcriptional profiling approaches to determine the requirements of Spdef in stomach epithelial homeostasis. In wild-type mice, Spdef RNA and protein are expressed predominantly in mucous gland cells of the antrum and in mucous neck cells of the glandular corpus. Within 1.5 years, nearly half of homozygous mutant mice developed profound mucosal hyperplasia of the gastric antrum. Submucosal infiltration of inflammatory cells preceded antral hyperplasia by several weeks. The absence of Spdef impaired terminal maturation of antral mucous gland cells, as reflected in reduced expression of Muc6 and Tff2 and reduced numbers of secretory granules. Antral gene expression abnormalities overlapped significantly with those in Spdef(-/-) colon, including genes implicated in secretory granule traffic and functions. Spdef is required for terminal maturation of antral mucous gland cells to protect animals from gastric inflammation and resulting hyperplasia. These requirements parallel Spdef functions in secretory intestinal cells and suggest a common molecular mechanism for maturation of gastrointestinal secretory lineages.


Assuntos
Glândulas Exócrinas/metabolismo , Regulação da Expressão Gênica , Muco/metabolismo , Proteínas Proto-Oncogênicas c-ets/metabolismo , Antro Pilórico/metabolismo , Animais , Glândulas Exócrinas/patologia , Homeostase , Hiperplasia , Camundongos , Camundongos Knockout , Mucina-6/genética , Mucina-6/metabolismo , Mucinas/genética , Mucinas/metabolismo , Proteínas Musculares/genética , Proteínas Musculares/metabolismo , Especificidade de Órgãos , Peptídeos/genética , Peptídeos/metabolismo , Proteínas Proto-Oncogênicas c-ets/genética , Antro Pilórico/patologia , Fator Trefoil-2
11.
Res Microbiol ; 158(6): 501-5, 2007.
Artigo em Inglês | MEDLINE | ID: mdl-17566711

RESUMO

TfxG, one of the tfxABCDEFG cluster genes that code for trifolitoxin (TFX) production, was initially described in Rhizobium leguminosarum bv. trifolii T24. Although several genes in the tfx family have functions related to TFX production or resistance to TFX, the function of tfxG is largely unknown. Using cDNA-amplified fragment length polymorphism (cDNA-AFLP) analysis, we found that expression of the tfxG gene dramatically increased under alkaline culture conditions in Sinorhizobium meliloti CCBAU 81024. This result was confirmed by northern blot analysis. Mutagenesis of tfxG significantly decreased the viability of Sinorhizobium meliloti CCBAU 81024 under alkali stress. Complementation of the tfxG mutant strain using the functional tfxG gene recovered its alkali tolerance to a wild-type level. Genomic analysis of the tfxG gene suggests that choline and homoserine kinase domains may contribute to its alkali tolerance function. This is the first clear evidence that tfxG plays a crucial role in the alkali tolerance of S. meliloti CCBAU 81024, and the finding provides its biological function.


Assuntos
Concentração de Íons de Hidrogênio , Peptídeos/genética , Sinorhizobium meliloti/crescimento & desenvolvimento , Bacteriocinas/genética , Cinética , Sinorhizobium meliloti/genética
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