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Quinones represent a class of crude organic compounds ubiquitously distributed in nature. Their distinctive quinone-type structure confers upon them unique properties and applications. Quinones demonstrate significant biological activities, including antioxidant, antimicrobial, and antitumor properties. Additionally, they demonstrate noteworthy physicochemical characteristics, including excellent dyeing properties and stability. Given their diverse qualities, quinones hold significant promise for applications in industrial manufacturing, healthcare, and food production, thus garnering considerable attention in recent years. While there is a growing body of research on quinones, the existing literature falls short of providing a comprehensive review encompassing recent advancements in this field along with established knowledge. This paper offers a comprehensive review of research progress for quinones, encompassing structural classification, source synthesis, extraction methods, properties, functions, and specific applications. It serves as a reference and theoretical foundation for the further development and utilization of quinones.
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Chronic inflammation is a common foundation for the development of many non-communicable diseases, particularly diabetes, atherosclerosis, and tumors. The activation of the axis involving Advanced Glycation End products (AGEs) and their receptor RAGE is a key promotive factor in the chronic inflammation process, influencing the pathological progression of these diseases. The accumulation of AGEs in the body results from an increase in glycation reactions and oxidative stress, especially pronounced in individuals with diabetes. By binding to RAGE, AGEs activate signaling pathways such as NF-κB, promoting the release of inflammatory factors, exacerbating cell damage and inflammation, and further advancing the formation of atherosclerotic plaques and tumor development. This review will delve into the molecular mechanisms by which the AGEs-RAGE axis activates chronic inflammation in the aforementioned diseases, as well as strategies to inhibit the AGEs-RAGE axis, aiming to slow or halt the progression of chronic inflammation and related diseases. This includes the development of AGEs inhibitors, RAGE antagonists, and interventions targeting upstream and downstream signaling pathways. Additionally, the early detection of AGEs levels and RAGE expression as biomarkers provides new avenues for the prevention and treatment of diabetes, atherosclerosis, and tumors.
Assuntos
Produtos Finais de Glicação Avançada , Inflamação , Receptor para Produtos Finais de Glicação Avançada , Transdução de Sinais , Humanos , Produtos Finais de Glicação Avançada/metabolismo , Receptor para Produtos Finais de Glicação Avançada/metabolismo , Inflamação/metabolismo , Animais , Anti-Inflamatórios/uso terapêutico , Aterosclerose/metabolismo , Aterosclerose/patologiaRESUMO
Lactobacillus fermentum (L. fermentum) was first evaluated as a potential advanced glycation end-product (AGE) formation inhibitor by establishing a bovine serum albumin (BSA) + glucose (glu) glycation model in the present study. The results showed that the highest inhibition rates of pentosidine and total fluorescent AGEs by L. fermentum were approximately 51.67% and 77.22%, respectively, which were higher than that of aminoguanidine (AG). Mechanistic analysis showed that L. fermentum could capture methylglyoxal and glyoxal, inhibit carbonyl and sulfhydryl oxidation, reduce the binding of glucose and amino groups, increase total phenolic content and antioxidant activity, and release intracellular substances to scavenge free radicals; these abilities were the basis of the antiglycation mechanism of L. fermentum. In addition, L. fermentum significantly prevented conformational changes in proteins during glycation, reduced protein cross-linking by 35.67%, and protected the intrinsic fluorophore. Therefore, the inhibition of L. fermentum on glycation mainly occurs through antioxidation, the capture of dicarbonyl compounds, and the protection of the BSA structure. These findings collectively suggest that Lactobacillus is an inhibitor of protein glycation and AGE formation and has the potential for nutraceutical applications.
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As lignocellulose recalcitrance principally restricts for a cost-effective conversion into biofuels and bioproducts, this study re-selected the brittle stalk of corn mutant by MuDR-transposon insertion, and detected much reduced cellulose polymerization and crystallinity. Using recyclable CaO chemical for biomass pretreatment, we determined a consistently enhanced enzymatic saccharification of pretreated corn brittle stalk for higher-yield bioethanol conversion. Furthermore, the enzyme-undigestible lignocellulose was treated with two-step thermal-chemical processes via FeCl2 catalysis and KOH activation to generate the biochar with significantly raised adsorption capacities with two industry dyes (methylene blue and Congo red). However, the desirable biochar was attained from one-step KOH treatment with the entire brittle stalk, which was characterized as the highly-porous nanocarbon that is of the largest specific surface area at 1697.34 m2/g and 2-fold higher dyes adsorption. Notably, this nanocarbon enabled to eliminate the most toxic compounds released from CaO pretreatment and enzymatic hydrolysis, and also showed much improved electrochemical performance with specific capacitance at 205 F/g. Hence, this work has raised a mechanism model to interpret how the recalcitrance-reduced lignocellulose is convertible for high-yield bioethanol and multiple-function biochar with high performance.
Assuntos
Celulose , Carvão Vegetal , Zea mays , Celulose/química , Zea mays/química , Polimerização , CorantesRESUMO
The use of frozen dough is an intensive food-processing practice that contributes to the development of chain operations in the bakery industry. However, the fermentation activity of yeasts in frozen dough can be severely damaged by freeze-thaw stress, thereby degrading the final bread quality. In this study, chickpea protein hydrolysate significantly improved the quality of steamed bread made from frozen dough while enhancing the yeast survival rate and maintaining yeast cell structural integrity under freeze-thaw stress. The mechanism underlying this protective role of chickpea protein hydrolysate was further investigated by untargeted metabolomics analysis, which suggested that chickpea protein hydrolysate altered the intracellular metabolites associated with central carbon metabolism, amino acid synthesis, and lipid metabolism to improve yeast cell freeze-thaw tolerance. Therefore, chickpea protein hydrolysate is a promising natural antifreeze component for yeast cryopreservation in the frozen dough industry.
Assuntos
Cicer , Proteínas de Saccharomyces cerevisiae , Saccharomyces cerevisiae/metabolismo , Cicer/metabolismo , Hidrolisados de Proteína/metabolismo , Congelamento , Proteínas de Saccharomyces cerevisiae/metabolismo , Fermentação , Pão/análiseRESUMO
Procyanidin-amino acid interactions during transmembrane transport cause changes in the structural and physical properties of peptides, which limits further absorption of oligopeptide-advanced glycation end products (AGEs). In this study, glycated casein hydrolysates (GCSHs) were employed to investigate the structure and interaction mechanism of GCSH with lotus seedpod oligomeric procyanidin (LSOPC) complexes in an intestinal environment. LSOPC can interact with GCSH under certain conditions to form hydrogen bonds and hydrophobic interactions to form GCSH-LSOPC complexes. Results showed that procyanidin further leads to the transformation of a GCSH secondary structure and the increase of surface hydrophobicity (H0). The strongest non-covalent interaction between GCSH and (-)-epigallocatechin gallate (EGCG) was due to the polyhydroxy structure of EGCG. Binding site analysis showed that EGCG binds to the internal cavity of P1 to maintain the relative stability of the binding conformation. The antioxidant capacity of GCSH was remarkably elevated by GCSH-LSOPC. This study will provide a new reference for the accurate control of oligopeptide-AGEs absorption by LSOPC in vivo.
Assuntos
Catequina , Lotus , Proantocianidinas , Caseínas/análise , Extratos Vegetais/química , Proantocianidinas/química , Lotus/química , Antioxidantes/análise , Catequina/química , Produtos Finais de Glicação Avançada/metabolismo , Sementes/química , DigestãoRESUMO
Research on advanced glycation end product (AGEs) inhibition has generally focused on food processing, but many protein-AGEs will still be taken. Oligopeptide (OLP)-AGEs, as the main form after digestion, will damage human health once absorbed. Here, we investigated the ability of lotus seedpod oligomeric procyanidins (LSOPC) to inhibit the absorption of the OLP-AGEs and elucidated the underlying mechanism. Our results showed that the inhibition rate of LSOPC on the absorption of OLP-AGEs was about 50 ± 5.38%. 0.1, 0.2, and 0.3 mg/mL could upregulate the expression of ZO-1 and downregulate the expression of PepT1 and clathrin. Molecular docking showed that LSOPC could compete with the binding of OLP-AGEs to PepT1 and AP-2, thus inhibiting the absorption of OLP-AGEs. Furthermore, the interaction of LSOPC with the OLP-AGEs reduced the surface hydrophobicity of OLP-AGEs. It altered the secondary structure of the OLP-AGEs, thus weakening the affinity of the OLP-AGEs to the transporter protein to inhibit the absorption of OLP-AGEs. Together, our data revealed potential mechanisms by which LSOPC inhibit the absorption of OLP-AGEs and opened up new perspectives on the application of LSOPC in reducing the increasing health risks posed by OLP-AGEs.
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Lotus , Proantocianidinas , Humanos , Proantocianidinas/química , Lotus/química , Simulação de Acoplamento Molecular , Extratos Vegetais/química , Produtos Finais de Glicação Avançada/química , Sementes/químicaRESUMO
Accumulation of advanced glycation end products (AGEs) is linked with development or aggravation of many degenerative processes or disorders. Fruit vinegars are rich in polyphenols that can be a good dietary source of AGEs inhibitors. In this study, eight kinds of vinegars were prepared. Among them, the highest polyphenol and flavonoid content were orange vinegar and kiwi fruit vinegar, respectively. Ferulic acid, vanillic acid, chlorogenic acid, p-coumaric acid, caffeic acid, catechin, and epicatechin were main polyphenols in eight fruit vinegars. Then, we measured the inhibitory effect of eight fruit vinegars on fluorescent AGEs, and found that orange vinegar had the highest inhibitory rate. Data here suggested that orange vinegar and its main components catechin, epicatechin, and p-coumaric acid could effectively reduce the level of ROS, RAGE, NADPH and inflammatory factors in Caco-2 cells. Our research provided theoretical basis for the application of orange vinegar as AGEs inhibitor.
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Advanced glycation end-products (AGEs) are the final products of the non-enzymatic interaction between reducing sugars and amino groups in proteins, lipids and nucleic acids. In numerous diseases, such as diabetes, neuropathy, atherosclerosis, aging, nephropathy, retinopathy, and chronic renal illness, accumulation of AGEs has been proposed as a pathogenic mechanism of inflammation, oxidative stress, and structural tissue damage leading to chronic vascular issues. Current studies on the inhibition of AGEs mainly focused on food processing. However, there are few studies on the inhibition of AGEs during digestion, absorption and metabolism although there are still plenty of AGEs in our body with our daily diet. This review comprehensively expounded AGEs inhibition mechanism based on the whole process of digestion, absorption and metabolism by polyphenols, amino acids, hydrophilic colloid, carnosine and other new anti-glycation agents. Our study will provide a ground-breaking perspective on mediation or inhibition AGEs.
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Diabetes Mellitus , Reação de Maillard , Humanos , Produtos Finais de Glicação Avançada/metabolismo , Estresse Oxidativo , Digestão , Receptor para Produtos Finais de Glicação Avançada/metabolismoRESUMO
Glycation of protein results in the formation of advanced glycation end-products (AGEs), which are further absorbed by the body through digestion in the gastrointestinal tract. The inhibitory properties of procyanidin for the release of AGEs from glycated proteins are of great significance in promoting, accelerating or stabilizing gastrointestinal folding intermediates, although the mechanism of action remains unclear. With the background of dairy processing, the study investigated the inhibitory effect of lotus seedpod oligomeric procyanidins (LSOPC) and its three monomers on AGE release from glycated casein (G-CS) during gastrointestinal digestion. In gastrointestinal microenvironments, multispectral and microscopy analysis were used to investigate interaction mechanisms. Results showed that the binding force of the protein-procyanidin complexes were hydrogen bonding and hydrophobic interaction and LSOPC leaded the G-CS secondary structure transformations furtherly. In the gastric environment, all monomers displayed stronger binding to pepsin but in the intestinal environment, results were opposite. Molecular docking showed that procyanidins were bound in the internal cavity of G-CS, pepsin and pancreatin, thereby forming a relatively stable binding conformation. Moreover, procyanidins enhanced the antioxidant capacity of G-CS, which could attenuate postprandial oxidative stress in the gastrointestinal tract caused by the release of AGEs. Together, this study improves our understanding of dietary AGEs during gastrointestinal digestion.
Assuntos
Lotus , Proantocianidinas , Biflavonoides , Caseínas/análise , Catequina , Digestão , Lotus/química , Simulação de Acoplamento Molecular , Proantocianidinas/química , Sementes/químicaRESUMO
This study investigated the modulatory effects of lotus seedpod oligomeric procyanidins (LSOPC) on the advanced glycation endproducts (AGEs)-induced liver injury via advanced glycation end-product receptors (RAGE)-mitogen-activated protein kinases (MAPK)-nuclear factor-kappa B (NF-κB) signaling pathways in a mice model. To examine the antioxidation properties of LSOPC, a model of high-AGEs-diet were established using Sprague Dawley (SD) male mice fed with a normal AIN-93G diet, a high AGEs diet (H), or H plus 0.5 or 0.2% (w/w) LSOPC for 12 weeks. Our results showed that LSOPC inhibited the AGEs formation and alleviated AGEs-induced liver injury by suppressing the nuclear translocation of NF-κB and activation of the MAPK signaling pathway. Additionally, LSOPC inhibited the genes expression of tumor necrosis factor-α (TNF-α) and interleukin 6 (IL-6). Taken together, LSOPC treatment potentially inhibited the AGEs formation and modulated liver injury with long-term dietary AGEs by suppressing RAGE-MAPK-NF-κB pathways.
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Biflavonoides/metabolismo , Catequina/metabolismo , Dieta , Produtos Finais de Glicação Avançada/efeitos dos fármacos , Lotus/embriologia , NF-kappa B/metabolismo , Proantocianidinas/metabolismo , Receptor para Produtos Finais de Glicação Avançada/metabolismo , Sementes/metabolismo , Transdução de Sinais , Animais , CamundongosRESUMO
Glycated proteins are the main source of dietary advanced glycation end products (AGEs). Glycated proteins are enzymatically hydrolyzed in the gastrointestinal tract, which releases more absorbable and smaller potentially harmful AGEs. This study investigated the inhibitory effect of catechin on AGE release from glycated bovine serum albumin (G-BSA) during gastrointestinal digestion. Catechin inhibited AGE release during gastrointestinal digestion, especially in the gastric digestion stage. Additionally, catechin altered these peptides in the small intestine by reducing G-BSA digestibility. The proposed mechanism involves interactions between catechin and G-BSA/digestive enzymes, inhibiting digestive enzyme activity and changing the conformation of G-BSA. Catechin reduced G-BSA ß-sheet content and protected the helical conformation. Moreover, catechin enhanced the antioxidant capacity of G-BSA, which could attenuate postprandial oxidative stress in the gastrointestinal tract caused by the release of AGEs. This study improves our understanding of the nutritional and health effects of catechin on dietary AGEs during gastrointestinal digestion.
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Catequina , Digestão , Produtos Finais de Glicação Avançada , Soroalbumina Bovina , Catequina/metabolismo , Produtos Finais de Glicação Avançada/metabolismo , PeptídeosRESUMO
Lactobacillus enriched with organic/inorganic selenium and pickles fermented with the Lactobacillus plantarum R were prepared. The results showed that selenium-enriched Lactobacillus plantarum R enhanced the antioxidant capacity, inhibition rate of advanced glycation end-products (AGEs), nitrite degradation, and the organic acid production of fermented pickles, while Lactobacillus plantarum R enriched with inorganic selenium (R-Se-IN) showed the best performance. Twenty-three aroma-active substances and seven characteristic compounds were detected in the R-Se-IN group. Moreover, the bacterial community result revealed that Lactococcus, Lactobacillus, and Leuconostoc were predominant in the R-Se-IN group, while the other groups contained Enterobacter, Halomonas, and Klebsiella. Furthermore, the correlations between environmental factors, differential flavor substances, and microbial communities were explored based on multivariate statistical analysis. These results indicate that the addition of Lactobacillus plantarum R enriched with organic/inorganic selenium influenced the environmental factors, differential flavor substances, and microbial communities of the fermented pickles.
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Alimentos Fermentados , Lactobacillus plantarum , Microbiota , Selênio , Fermentação , LactobacillusRESUMO
Salmonella typhimurium DT104 infection causes the death of Caenorhabditis elegans, which can be prevented by certain Lactobacillus isolates. However, the molecular mechanisms of both the host response to the infection and the protection by Lactobacillus are largely unclear. The present study has investigated the life-span and gene expression of both wild-type (WT) and mutants in some key components of cell signaling in response to S. typhimurium infection and protection from Lactobacillus zeae. The results indicated that the gene expression of daf-16 in the DAF/ insulin-like growth factor (DAF/IGF) pathway, ced-3 and ced-9 in the programmed cell death (PCD) pathway, lys-7, spp-1, and abf-3 for antimicrobial peptide production, and bar-1 involved in the production of other defense molecules was all significantly upregulated when the wild-type (WT) was subjected to DT104 infection. On the contrary, the gene expression of tir-1, sek-1, and pmk-1 in the p38 mitogen-activated protein kinase (MAPK) pathway and clec-60, sod-3, and skn-1 for the production of other defense molecules was significantly suppressed by DT104. Pretreatment of the worms with L. zeae LB1 significantly upregulated the expression of almost all the tested genes except for ced-3, ced-9, abf-2, age-1, and dbl-1 compared with the nematode infected with DT104 only. Mutants defective in the cell signaling or other defense molecules of C. elegans were either more susceptible (defective in nsy-1, sek-1, pmk-1, ced-3, ced-9, skn-1, or daf-16) or more resistant (defective in age-1 or dbl-1) to DT104 infection than the WT except for the mutant defective in sod-3. Mutants defective in antimicrobial peptides (lys-7 or abf-3) were also more susceptible than the WT. In contrast, the mutant defective in spp-1 became more resistant. When all the mutants were pretreated with L. zeae LB1, five mutants that are defective in nsy-1, sek-1, pmk-1, abf-3, or lys-7 showed no response to the protection from LB1. These results suggest that L. zeae LB1 can regulate C. elegans cell signaling including the p38 MAPK pathway and downstream production of antimicrobial peptides and defense molecules to combat Salmonella infection.
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Lactobacillus/imunologia , Sistema de Sinalização das MAP Quinases/imunologia , Probióticos/administração & dosagem , Infecções por Salmonella/prevenção & controle , Salmonella typhimurium/imunologia , Animais , Animais Geneticamente Modificados , Caenorhabditis elegans/imunologia , Caenorhabditis elegans/microbiologia , Proteínas de Caenorhabditis elegans/genética , Proteínas de Caenorhabditis elegans/metabolismo , Modelos Animais de Doenças , Sistema de Sinalização das MAP Quinases/genética , Proteínas Citotóxicas Formadoras de Poros/metabolismo , Infecções por Salmonella/imunologia , Infecções por Salmonella/microbiologia , Proteínas Quinases p38 Ativadas por Mitógeno/genética , Proteínas Quinases p38 Ativadas por Mitógeno/metabolismoRESUMO
Advanced glycation end products (AGEs) and their important intermediate products (α-dicarbonyl compounds) that are generated by the Maillard reaction are closely related to diabetes. Our study first investigated the mechanisms of the anti-glycation effects of epicatechin (EC), (-)-epicatechin gallate (ECG), (-)-epigallocatechin (EGC), and (-)-epigallocatechin gallate (EGCG) in an alcoholic environment. The results showed that catechins played an important role in the inhibition of AGE formation, and the effect of EC was the best. Their corresponding mechanisms included total antioxidant capacity (TAOC), 1,1-diphenyl-2-picrylhydrazyl (DPPH) scavenging ability, trapping of methylglyoxal (MGO), protection of the protein structure, and inhibition of the activities of α-amylase, α-glucosidase, and ß-glucosidase, which were consistent with the study of molecular docking. This study will offer a theoretical basis for the applications of different types of catechins to alcoholic beverages as natural AGE formation inhibitors.
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Catequina/química , Catequina/metabolismo , Produtos Finais de Glicação Avançada/química , Produtos Finais de Glicação Avançada/metabolismo , Antioxidantes/farmacologia , Sítios de Ligação/efeitos dos fármacos , Compostos de Bifenilo , Catequina/análogos & derivados , Catequina/farmacologia , Glucosidases/efeitos dos fármacos , Glicosilação , Simulação de Acoplamento Molecular , Picratos , Aldeído Pirúvico , alfa-Amilases/efeitos dos fármacos , alfa-Glucosidases/metabolismoRESUMO
Catechin, a natural antiglycative agent, was incorporated into fermented vinegar, and has high potential to lower the risk of diabetes. In this study, vinegar containing 5% catechin as a substrate for acetous fermentation significantly inhibited the formation of total fluorescent advanced glycation end-products (AGEs), as well as Nε-(carboxymethyl)lysine (CML)/Nε-(carboxyethyl)lysine (CEL), especially when added during acetic fermentation. Further study proved that catechin could not only significantly suppress the increase of blood glucose levels, but also inhibit α-amylase, α-glucosidase and ß-glucosidase strongly with IC50 values of 0.533 mg mL-1, 0.307 mg mL-1 and 0.413 mg mL-1, respectively. Moreover, 32 volatile compounds were finally identified by headspace solid phase microextraction gas chromatography-mass spectrometry (HSPM-GC-MS) and electronic nose. The flavor of the catechin-vinegars, which possess relatively high ester and low acid contents, was superior to that of traditional vinegar. Therefore, it was helpful to use catechin as a functional food ingredient in vinegar to prevent AGE-associated diseases and alleviate postprandial hyperglycemia, through limiting the digestion of starch and inhibiting the uptake of glucose. Meanwhile, the pleasant flavor and safety of catechin-vinegar were better than traditional vinegar, which represents prominent value to attract consumers.
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Ácido Acético/análise , Catequina/análise , Produtos Finais de Glicação Avançada/análise , Ácido Acético/metabolismo , Acetobacter/metabolismo , Fermentação , Aditivos Alimentares/análise , Tecnologia de Alimentos , Alimento Funcional/análise , Cromatografia Gasosa-Espectrometria de Massas , Saccharomyces cerevisiae/metabolismo , Microextração em Fase Sólida , Compostos Orgânicos Voláteis/análise , Compostos Orgânicos Voláteis/metabolismoRESUMO
Selenium (Se) is one of the essential trace elements in the human body, and Se-enriched lactic acid bacteria (LAB) can improve the biological utilization value of inorganic Se. The aim of this study was to isolate Se-enriched LAB and study their effects on antioxidant activity and nitrite degradation. The Se-enriched LAB L.P2, which was nitrite-tolerant and could grow in 30 µg/mL sodium selenite (Na2SeO3) medium, was isolated from the traditional fermented Chinese sauerkraut. L.P2 belonged to Lactobacillus plantarum according to the 16S rDNA analysis. The biomass and lactic acid production of L.P2 reached to a maximum (9.52 log CFU/mL and 16.99 mg/mL) when 2.0 µg/mL Na2SeO3 was supplemented in the medium. Additionally, the nitrite degradation rate reached 85.76% when the initial concentration of Na2SeO3 was 2.0 µg/mL. The Se-enriched LAB enhanced the scavenging capacity of hydroxyl radical and superoxide free radical of L.P2 and improved the lipid peroxidation and ion-chelating abilities. Moreover, the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) in Se 4 group (4.0 µg/mL Na2SeO3 was added) reached 48.49 and 50.35 U/mg, respectively. Thus, Se 4 concentration was significantly higher than that of Se 0 group (with no Se added). In particular, SOD and GSH-Px enzymes correlated with nitrite degradation (P < 0.01). Collectively, our results indicate that Se supplementation can enhance the antioxidant capacity of LAB, contribute to its nitrite degradation, and thus may have potential applications in functional foods.
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Antioxidantes/metabolismo , Suplementos Nutricionais , Lactobacillales/efeitos dos fármacos , Lactobacillales/metabolismo , Nitritos/metabolismo , Selênio/farmacologia , Brassica , Quelantes , DNA Ribossômico/análise , Tolerância a Medicamentos , Alimentos Fermentados/microbiologia , Glutationa Peroxidase/metabolismo , Humanos , Ácido Láctico/biossíntese , Lactobacillales/crescimento & desenvolvimento , Lactobacillales/isolamento & purificação , Nitritos/efeitos adversos , Filogenia , Selenito de Sódio/farmacologia , Superóxido Dismutase/metabolismoRESUMO
Nonenzymatic glycosylation (NEG) can generate advanced glycation end products (AGEs) and its intermediates α-dicarbonyl compounds, which contribute to the risk of diabetes. This study investigated the anti-glycation mechanisms and structure-activity relationship of (+)-catechin (CC) and (-)-epicatechin (EC). The results showed that the effect of CC on inhibiting AGEs was significantly better than that of EC (pâ¯<â¯0.05). By exploring the mechanism, we found that there was no significant difference in the ability of CC and EC to capture α-dicarbonyl compounds. But CC was found to be more efficient than EC to inhibit RO, OH and CHO radicals generation, which may be the primary reason that CC was more effective than EC on AGEs inhibition. What's more, CC showed better inhibitory effect on ß-glucosidase that was close to the molecular docking study. Our results will provide a theoretical foundation for development of different structure of procyanidins as natural AGEs inhibitors in food and medicine.
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Biflavonoides/química , Catequina/química , Produtos Finais de Glicação Avançada/química , Proantocianidinas/química , Biflavonoides/metabolismo , Sítios de Ligação , Catequina/metabolismo , Cromatografia Líquida de Alta Pressão , Produtos Finais de Glicação Avançada/metabolismo , Glioxal/química , Humanos , Simulação de Acoplamento Molecular , Proantocianidinas/metabolismo , Estrutura Terciária de Proteína , Relação Estrutura-Atividade , Espectrometria de Massas em Tandem , alfa-Amilases/antagonistas & inibidores , alfa-Amilases/metabolismo , beta-Glucosidase/antagonistas & inibidores , beta-Glucosidase/metabolismoRESUMO
Enterotoxigenic Escherichia coli (ETEC) infection causes the death of Caenorhabditis elegans, which can be prevented by certain Lactobacillus isolates. The host response of C. elegans to ETEC infection and its regulation by the isolates are, however, largely unclear. This study has revealed that, in agreement with the results of life-span assays, the expression of the genes encoding p38 mitogen-activated protein kinase (MAPK) pathway (nsy-1, sek-1, and pmk-1), insulin/insulin-like growth factor (DAF/IGF) pathway (daf-16), or antimicrobial peptides (lys-7, spp-1, and abf-3) and other defensing molecules (abf-2, clec-85) was upregulated significantly when the wild-type nematode (N2) was subjected to ETEC infection. This upregulation was further enhanced by the pretreatment with Lactobacillus zeae LB1, but not with L. casei CL11. Mutants defective in the cell signaling of C. elegans were either more susceptible (defective in NSY-1, SEK-1, PMK-1, or DAF16) or more resistant (defective in AGE-1, DBL-1, SKN-1, or SOD-3) to ETEC infection compared with the wild-type. Mutants defective in antimicrobial peptides (LYS-7, SPP1, or ABF-3) were also more susceptible. In addition, mutants that are defective in NSY-1, SEK-1, PMK-1, DAF16, ABF-3, LYS-7, or SPP1 showed no response to the protection from L. zeae LB1. The expression of the genes encoding antimicrobial peptides (lys-7, spp-1, and abf-3) and other defensing molecules (abf-2, clec-60, and clec-85) were almost all upregulated in AGE-1- or DBL-1-defective mutant compared with the wild-type, which was further enhanced by the pretreatment of L. zeae LB1. The expression of these genes was, however, mostly downregulated in NSY-1- or DAF-16-defective mutant. These results suggest that L. zeae LB1 regulates C. elegans signaling through the p38 MAPK and DAF/IGF pathways to control the production of antimicrobial peptides and defensing molecules to combat ETEC infection.
Assuntos
Antibiose , Caenorhabditis elegans/microbiologia , Caenorhabditis elegans/fisiologia , Escherichia coli Enterotoxigênica/fisiologia , Infecções por Escherichia coli/microbiologia , Interações Hospedeiro-Patógeno , Lactobacillus/fisiologia , Transdução de Sinais , Animais , Peptídeos Catiônicos Antimicrobianos/genética , Peptídeos Catiônicos Antimicrobianos/metabolismo , Biomarcadores , Resistência à Doença , Infecções por Escherichia coli/genética , Infecções por Escherichia coli/metabolismo , Perfilação da Expressão Gênica , Imunomodulação , Probióticos , Proteínas Quinases p38 Ativadas por Mitógeno/metabolismoRESUMO
Herpes simplex virus type 1 (HSV-1), a member of the Herpes viridae, is associated with a wide variety of nervous system diseases including meningitis and encephalitis. The data presented here demonstrate that miR-649 promotes the replication of HSV-1 without affecting cell viability. Further mechanistic studies revealed that MALT1 (mucosa associated lymphoid tissue lymphoma translocation gene 1) is directly targeted by miR-649. We then found that MALT1 and the downstream NF-κB signaling pathway, are involved in miR-649-induced HSV-1 replication. Interestingly, miR-649 levels were downregulated after HSV-1 infection, and miR-649 expression was negatively associated with MALT1 expression in HSV-1-infected HeLa cells. Taken together, this present study indicates that miR-649 promotes HSV-1 replication through regulation of the MALT1-mediated antiviral signaling pathway and suggests a promising target for antiviral therapies. J. Med. Virol. 89:1069-1079, 2017. © 2016 Wiley Periodicals, Inc.