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1.
Food Chem ; 341(Pt 1): 128148, 2020 Sep 22.
Artículo en Inglés | MEDLINE | ID: mdl-33038776

RESUMEN

The brown seaweed Undaria pinnatifida polysaccharides show various biological activities, but their hypoglycemic activity and the underlying mechanism remain unclear. Here, three fractions of sulfated polysaccharides Up-3, Up-4, and Up-5 were prepared by microwave-assisted extraction from U. pinnatifida. In vitro assays demonstrated that Up-3 and Up-4 had strong α-glucosidase inhibitory activity, and Up-3, Up-4, and Up-5 could improve the glucose uptake in insulin-resistant HepG2 cells without affecting their viability. In vivo studies indicated Up-3 and Up-4 markedly reduced postprandial blood glucose levels. Up-U (a mixture of Up-3, Up-4, and Up-5), reduced fasting blood glucose levels, increased glucose tolerance and alleviated insulin resistance in HFD/STZ-induced hyperglycemic mice. Histopathological observation and hepatic glycogen measurement showed that Up-U alleviated the damage of the pancreas islet cell, reduced hepatic steatosis, and promoted hepatic glycogen synthesis. These findings suggest that Up-U could alleviate postprandial and HFD/STZ-induced hyperglycemia and was a potential agent for diabetes treatment.

2.
Mar Drugs ; 18(9)2020 Aug 27.
Artículo en Inglés | MEDLINE | ID: mdl-32867177

RESUMEN

A low fasting blood glucose level is a common symptom in diabetes patients and can be induced by high-fat diet (HFD) feeding at an early stage, which may play important roles in the development of diabetes, but has received little attention. In this study, five polysaccharides were prepared from Sargassumfusiforme and their effects on HFD-induced fasting hypoglycemia and gut microbiota dysbiosis were investigated. The results indicated that C57BL/6J male mice fed an HFD for 4 weeks developed severe hypoglycemia and four Sargassumfusiforme polysaccharides (SFPs), consisting of Sf-2, Sf-3, Sf-3-1, and Sf-A, significantly prevented early fasting hypoglycemia without inducing hyperglycemia. Sf-1 and Sf-A could also significantly prevent HFD-induced weight gain. Sf-2, Sf-3, Sf-3-1, and Sf-A mainly attenuated the HFD-induced decrease in Bacteroidetes, and all five SFPs had a considerable influence on the relative abundance of Oscillospira, Mucispirillum, and Clostridiales. Correlation analysis revealed that the fasting blood glucose level was associated with the relative abundance of Mucispinllum and Oscillospira. Receiver operating characteristic analysis indicated that Mucispinllum and Oscillospira exhibited good discriminatory power (AUC = 0.745-0.833) in the prediction of fasting hypoglycemia. Our findings highlight the novel application of SFPs (especially Sf-A) in glucose homeostasis and the potential roles of Mucispinllum and Oscillospira in the biological activity of SFPs.

3.
J Microbiol ; 58(8): 716-723, 2020 Aug.
Artículo en Inglés | MEDLINE | ID: mdl-32524342

RESUMEN

Human cytomegalovirus (hCMV) is a ubiquitous herpesvirus, which results in the establishment of a latent infection that persists throughout the life of the host and can be reactivated when the immunity is low. Currently, there is no vaccine for hCMV infection, and the licensed antiviral drugs mainly target the viral enzymes and have obvious adverse reactions. Thus, it is important to search for compounds with anti-hCMV properties. The present study aimed to investigate the suppressive effects of piceatannol on hCMV Towne strain infection and the putative underlying mechanisms using human diploid fibroblast WI-38 cells. Piceatannol supplementation prevented the lytic changes induced by hCMV infection in WI-38 cells. Furthermore, piceatannol suppressed the expression of hCMV immediate-early (IE) and early (E) proteins as well as the replication of hCMV DNA in a dose-dependent manner. Moreover, hCMV-induced cellular senescence was suppressed by piceatannol, as shown by a decline in the senescence-associated ß-galactosidase (SA-ß-Gal) activity and decreased production of intracellular reactive oxygen species (ROS). p16INK4a, a major senescence-associated molecule, was dramatically elevated by current hCMV infection that was attenuated by pre-incubation with piceatannol in a dose-dependent manner. These results demonstrated that piceatannol suppressed the hCMV infection via inhibition of the activation of p16INK4a and cellular senescence induced by hCMV. Together, these findings indicate piceatannol as a novel and potent anti-hCMV agent with the potential to be developed as an effective treatment for chronic hCMV infection.

4.
J Cell Physiol ; 234(7): 11140-11148, 2019 07.
Artículo en Inglés | MEDLINE | ID: mdl-30537139

RESUMEN

Tamoxifen treatment is important assistant for estrogen-receptor-positive breast cancer (BRCA) after resection. This study aimed to identify signatures for predicting the prognosis of patients with BRCA after tamoxifen treatment. Data of gene-specific DNA methylation (DM), as well as the corresponding clinical data for the patients with BRCA, were obtained from The Cancer Genome Atlas and followed by systematic bioinformatics analyses. After mapping these DM CPG sites onto genes, we finally obtained 352 relapse-free survival (RFS) associated DM genes, with which 61,776 gene pairs were combined, including 1,614 gene pairs related to RFS. An 11 gene-pair signature was identified to cluster the 189 patients with BRCA into the surgical low-risk group (136 patients) and high-risk group (53 patients). Then, we further identified a tamoxifen-predictive signature that could classify surgical high-risk patients with significant differences on RFS. Combining surgical-only prognostic signature and tamoxifen-predictive signature, patients were clustered into surgical-only low-risk group, tamoxifen nonbenefit group, and tamoxifen benefit group. In conclusion, we identified that the gene pair PDHA2-APRT could serve as a potential prognostic biomarker for patients with BRCA after tamoxifen treatment.


Asunto(s)
Neoplasias de la Mama/tratamiento farmacológico , Neoplasias de la Mama/cirugía , Receptores Estrogénicos/metabolismo , Tamoxifeno/uso terapéutico , Neoplasias de la Mama/genética , Metilación de ADN , Femenino , Regulación Neoplásica de la Expresión Génica , Predisposición Genética a la Enfermedad , Humanos , Persona de Mediana Edad , Pronóstico , Análisis de Supervivencia
5.
Mediators Inflamm ; 2014: 930894, 2014.
Artículo en Inglés | MEDLINE | ID: mdl-25214720

RESUMEN

Increasing evidence has demonstrated that reactive oxygen species (ROS) induces oxidative stress and plays a crucial role in the pathogenesis of acute pancreatitis (AP). Hydrogen-rich saline (HRS), a well-known ROS scavenger, has been shown to possess therapeutic benefit on AP in many animal experiments. Recent findings have indicated that the NOD-like receptor family, pyrin domain-containing 3 (NLRP3) inflammasome, an intracellular multiprotein complex required for the maturation of interleukin- (IL-) 1ß, may probably be a potential target of HRS in the treatment of AP. Therefore, in this study, we evaluated the activation of NLRP3 inflammasome and meanwhile assessed the degree of oxidative stress and inflammatory cascades, as well as the histological alterations in mice suffering from cerulein-induced AP after the treatment of HRS. The results showed that the activation of NLRP3 inflammasome in AP mice was substantially inhibited following the administration of HRS, which was paralleled with the decreased NF-κB activity and cytokines production, attenuated oxidative stress and the amelioration of pancreatic tissue damage. In conclusion, our study has, for the first time, revealed that inhibition of the activation of NLRP3 inflammasome probably contributed to the therapeutic potential of HRS in AP.


Asunto(s)
Inflamasomas/metabolismo , Pancreatitis/metabolismo , Enfermedad Aguda , Animales , Proteínas Portadoras/metabolismo , Masculino , Ratones , Ratones Endogámicos BALB C , Proteína con Dominio Pirina 3 de la Familia NLR , Estrés Oxidativo/fisiología
6.
Int Immunopharmacol ; 21(1): 220-4, 2014 Jul.
Artículo en Inglés | MEDLINE | ID: mdl-24836752

RESUMEN

Increasing evidence has recently demonstrated that soluble heparan sulfate (HS), a degradation product of extracellular matrix produced by elastase, plays a key role in the aggravation of acute pancreatitis (AP) and associated lung injury. However little is known about the detailed mechanism underlying HS-induced inflammatory cascade. Our previous work has provided a valuable clue that a large-conductance K(+) channel (MaxiK) was involved in the HS-stimulated activation of murine macrophages. Here we attempted to ask whether pharmacological inhibition of the MaxiK channel will exert beneficial effects on the treatment of AP and secondary lung injury. The protective effects of paxilline, a specific blocker of MaxiK, on rats against sodium taurocholate induced AP were evaluated. Our data showed that paxilline substantially attenuated AP and resultant lung injury, mainly by limiting the burst of inflammatory responses, as proven by decreased plasma concentrations of tumor necrosis factor-α and macrophage inflammatory protein-2, together with unimpaired pancreatic enzyme activities in rats suffering from AP. Compared with the therapeutic administration, pre-treatment of paxilline showed superior potential to slow down the progress of AP. Furthermore, AP rats received paxilline exhibited improved histopathologic alterations both in the pancreas and the lungs, and even lower lung MPO activity. Taken together, our study provides evidence that MaxiK is involved in the spread of inflammatory responses and the following lung injury during the attack of AP, indicating that this ion channel is a promising candidate as a therapeutic target for AP.


Asunto(s)
Hígado/efectos de los fármacos , Lesión Pulmonar/tratamiento farmacológico , Macrófagos/efectos de los fármacos , Pancreatitis Aguda Necrotizante/tratamiento farmacológico , Paxillin/administración & dosificación , Animales , Quimiocina CXCL2/sangre , Progresión de la Enfermedad , Humanos , Canales de Potasio de Gran Conductancia Activados por el Calcio/antagonistas & inhibidores , Hígado/patología , Pulmón/efectos de los fármacos , Pulmón/patología , Lesión Pulmonar/inducido químicamente , Lesión Pulmonar/complicaciones , Macrófagos/inmunología , Masculino , Ratones , Modelos Animales , Pancreatitis Aguda Necrotizante/inducido químicamente , Pancreatitis Aguda Necrotizante/complicaciones , Paxillin/farmacología , Ratas , Ratas Wistar , Ácido Taurocólico/administración & dosificación , Factor de Necrosis Tumoral alfa/sangre
7.
Immunology ; 141(3): 345-52, 2014 Mar.
Artículo en Inglés | MEDLINE | ID: mdl-24138091

RESUMEN

Increasing evidence has demonstrated that Toll-like receptor 4 (TLR4) -mediated systemic inflammatory response syndrome accompanied by multiple organ failure, is one of the most common causes of death in patients with severe acute pancreatitis. Recent reports have revealed that heparan sulphate (HS) proteoglycan, a component of extracellular matrices, potentiates the activation of intracellular pro-inflammatory responses via TLR4, contributing to the aggravation of acute pancreatitis. However, little is known about the participants in the HS/TLR4-mediated inflammatory cascades. Our previous work provided a clue that a membrane potassium channel (MaxiK) is responsible for HS-induced production of inflammatory cytokines. Therefore, in this report we attempted to reveal the roles of MaxiK in the activation of macrophages stimulated by HS. Our results showed that incubation of RAW264.7 cells with HS up-regulated MaxiK and TLR4 expression levels. HS could also activate MaxiK channels to promote the efflux of potassium ions from cells, as measured by the elevated activity of caspase-1, whereas this was significantly abolished by treatment with paxilline, a specific blocker of the MaxiK channel. Moreover, it was found that paxilline substantially inhibited HS-induced activation of several different transcription factors in macrophages, including nuclear factor-κB, p38 and interferon regulatory factor-3, followed by decreased production of tumour necrosis factor-α and interferon-ß. Taken together, our investigation provides evidence that the HS/TLR4-mediated intracellular inflammatory cascade depends on the activation of MaxiK, which may offer an important opportunity for a new approach in therapeutic strategies of severe acute pancreatitis.


Asunto(s)
Membrana Celular/efectos de los fármacos , Heparitina Sulfato/farmacología , Canales de Potasio de Gran Conductancia Activados por el Calcio/agonistas , Activación de Macrófagos/efectos de los fármacos , Macrófagos/efectos de los fármacos , Potasio/metabolismo , Animales , Caspasa 1/metabolismo , Línea Celular , Membrana Celular/inmunología , Membrana Celular/metabolismo , Inmunidad Innata/efectos de los fármacos , Factor 3 Regulador del Interferón/metabolismo , Interleucina-1beta/metabolismo , Canales de Potasio de Gran Conductancia Activados por el Calcio/metabolismo , Lipopolisacáridos/farmacología , Macrófagos/inmunología , Macrófagos/metabolismo , Potenciales de la Membrana , Ratones , FN-kappa B/metabolismo , Bloqueadores de los Canales de Potasio/farmacología , Transducción de Señal/efectos de los fármacos , Receptor Toll-Like 4/agonistas , Receptor Toll-Like 4/metabolismo , Factor de Necrosis Tumoral alfa/metabolismo , Regulación hacia Arriba , Proteínas Quinasas p38 Activadas por Mitógenos/metabolismo
8.
Acta Crystallogr Sect E Struct Rep Online ; 66(Pt 10): o2561, 2010 Sep 15.
Artículo en Inglés | MEDLINE | ID: mdl-21587547

RESUMEN

In the title compound, C(14)H(20)N(2)O(5)S·CH(4)O, the pyran-ose and pyridine rings are linked through an S atom. The pyran-ose ring has a normal chair conformation. An intra-molecular O-H⋯N hydrogen bond occurs. Inter-molecular O-H⋯O, N-H⋯O, O-H⋯N and weak C-H⋯O hydrogen bonding is present in the crystal structure.

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