Your browser doesn't support javascript.
Mostrar: 20 | 50 | 100
Resultados 1 - 20 de 62
Filtrar
Mais filtros










Tipo de estudo
Intervalo de ano de publicação
1.
Adv Mater ; : e1905210, 2019 Nov 12.
Artigo em Inglês | MEDLINE | ID: mdl-31714630

RESUMO

Chalcopyrite compound CuGaTe2 is the focus of much research interest due to its high power factor. However, its high intrinsic lattice thermal conductivity seriously impedes the promotion of its thermoelectric performance. Here, it is shown that through alloying of isoelectronic elements In and Ag in CuGaTe2 , a quinary alloy compound system Cu1- x Agx Ga0.4 In0.6 Te2 (0 ≤ x ≤ 0.4) with complex nanosized strain domain structure is prepared. Due to strong phonon scattering mainly by this domain structure, thermal conductivity (at 300 K) drops from 6.1 W m-1 K-1 for the host compound to 1.5 W m-1 K-1 for the sample with x = 0.4. As a result, the optimized chalcopyrite sample Cu0.7 Ag0.3 Ga0.4 In0.6 Te2 presents an outstanding performance, with record-high figure of merit (ZT) reaching 1.64 (at 873 K) and average ZT reaching 0.73 (between ≈300 and 873 K), which are ≈37 and ≈35% larger than the corresponding values for pristine CuGaTe2 , respectively, demonstrating that such domain structure arising from isoelectronic multielement alloying in chalcopyrite compound can effectively suppress its thermal conductivity and elevate its thermoelectric performance remarkably.

2.
Phytother Res ; 33(10): 2775-2782, 2019 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-31373419

RESUMO

Diabetic nephropathy (DN) is one of the major complications of diabetes mellitus. The progression of DN has been found to be associated with high glucose (HG)-induced oxidative stress and inflammation in diabetes mellitus. Eriodictyol is a flavonoid that possesses antioxidant and anti-inflammatory effects. However, the effect of eriodictyol on DN remains unknown. In the present study, we evaluated the role of eriodictyol in mesangial cells (MCs) in response to HG condition. The results showed that eriodictyol repressed cell proliferation of HG-stimulated MCs. Treatment with eriodictyol attenuated oxidative stress, which was evidenced by increased superoxide dismutase activity as well as decreased production of reactive oxygen species (ROS) and malondialdehyde. Besides, eriodictyol suppressed the expressions of two NADPH oxidase (NOX) isoforms, NOX2 and NOX4, which are responsible for the generation of ROS. Eriodictyol suppressed the production of extracellular matrix proteins including fibronectin and Collagen IV, as well as the secretion of inflammatory cytokines including TNF-α, IL-1ß, and IL-6 in HG-induced MCs. Moreover, the HG-induced activation of Akt/NF-κB pathway was mitigated by eriodictyol. In conclusion, eriodictyol protected MCs from HG stimulation though inhibition of Akt/NF-κB pathway.

3.
Chem Commun (Camb) ; 55(16): 2344-2347, 2019 Feb 19.
Artigo em Inglês | MEDLINE | ID: mdl-30724313

RESUMO

Commercial carbon fiber cloth treated at 450 °C in air (CFC-450) possesses low C[double bond, length as m-dash]O content, exhibiting outstanding oxygen evolution activity in 1.0 M KOH electrolyte with an overpotential of 224 mV at current density of 10 mA cm-2. Meanwhile, we observed an electrochemical corrosion phenomenon associated with the carbon fiber cloth electrocatalyst during the OER tests, especially under high static potentials.

4.
ACS Nano ; 13(2): 1694-1702, 2019 Feb 26.
Artigo em Inglês | MEDLINE | ID: mdl-30649862

RESUMO

The phase-controlled synthesis of metallic and ambient-stable 2D MX2 (M is Mo or W; X is S) with 1T octahedral coordination will endow these materials with superior performance compared with their semiconducting 2H coordination counterparts. We report a clean and facile route to prepare 1T-MoS2 and 1T-WS2 through hydrothermal processing under high magnetic fields. We reveal that the as-synthesized 1T-MoS2 and 1T-WS2 are ambient-stable for more than 1 year. Electrochemical measurements show that 1T-MoS2 performs much better than 2H-MoS2 as the anode for sodium ion batteries. These results can provide a clean and facile method to prepare ambient-stable 1T-phase MX2.

5.
Front Pharmacol ; 9: 1187, 2018.
Artigo em Inglês | MEDLINE | ID: mdl-30459606

RESUMO

Diabetic nephropathy (DN) is characterized by inflammatory responses and extracellular matrix (ECM) accumulation. Astilbin is an active natural compound and possesses anti-inflammatory activity. The aim of this study was to evaluate the anti-inflammatory effect of astilbin on high glucose (HG)-induced glomerular mesangial cells and the potential mechanisms. The results showed that HG induced cell proliferation of HBZY-1 cells in a time-dependent manner, and astilbin inhibited HG-induced cell proliferation. The expression and secretion of inflammatory cytokines, including interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-α), and ECM components, including collagen IV (Col IV) and fibronectin (FN), were induced by HG. Moreover, TGF-ß1 and CTGF were also induced by HG. The induction by HG on inflammatory response and ECM accumulation was inhibited after astilbin treatment. Astilbin treatment also attenuated HG-induced decrease in expression of matrix metalloproteinase (MMP)-2 and MMP-9. The TLR4/MyD88/NF-κB pathway was activated by HG, and the inhibitor of TLR4 exhibited the same effect to astilbin on reversing the induction of HG. TLR4 overexpression attenuated the effect of astilbin on HG-induced inflammatory cytokine production and ECM accumulation. The results suggested that astilbin attenuated inflammation and ECM accumulation in HG-induced rat glomerular mesangial cells via inhibiting the TLR4/MyD88/NF-κB pathway. This work provided evidence that astilbin can be considered as a potential candidate for DN therapy.

6.
Biol Res ; 51(1): 31, 2018 Sep 04.
Artigo em Inglês | MEDLINE | ID: mdl-30180910

RESUMO

BACKGROUND: miR-214 was demonstrated to be upregulated in models of renal disease and promoted fibrosis in renal injury independent of TGF-ß signaling in vivo. However, the detailed role of miR-214 in acute kidney injury (AKI) and its underlying mechanism are still largely unknown. METHODS: In this study, an I/R-induced rat AKI model and a hypoxia-induced NRK-52E cell model were used to study AKI. The concentrations of kidney injury markers serum creatinine, blood urea nitrogen, and kidney injury molecule-1 were measured. The expressions of miR-214, tumor necrosis factor-α, interleukin (IL)-1ß, IL-6, were detected by RT-qPCR. The protein levels of Bcl-2, Bax, Dickkopf-related protein 3, ß-catenin, c-myc, and cyclinD1 were determined by western blot. Cell apoptosis and caspase 3 activity were evaluated by flow cytometry analysis and caspase 3 activity assay, respectively. Luciferase reporter assay was used to confirm the interaction between miR-214 and Dkk3. RESULTS: miR-214 expression was induced in ischemia-reperfusion (I/R)-induced AKI rat and hypoxic incubation of NRK-52E cells. Overexpression of miR-214 alleviated hypoxia-induced NRK-52E cell apoptosis while inhibition of miR-214 expression exerted the opposite effect. Dkk3 was identified as a target of miR-214. Anti-miR-214 abolished the inhibitory effects of DKK3 knockdown on hypoxia-induced NRK-52E cell apoptosis by inactivation of Wnt/ß-catenin signaling. Moreover, miR-214 ameliorated AKI in vivo by inhibiting apoptosis and fibrosis through targeting Dkk3 and activating Wnt/ß-catenin pathway. CONCLUSION: miR-214 ameliorates AKI by inhibiting apoptosis through targeting Dkk3 and activating Wnt/ß-catenin signaling pathway, offering the possibility of miR-214 in the therapy of ischemic AKI.


Assuntos
Lesão Renal Aguda/metabolismo , Cateninas/metabolismo , Peptídeos e Proteínas de Sinalização Intercelular/metabolismo , MicroRNAs/metabolismo , Via de Sinalização Wnt/genética , Lesão Renal Aguda/induzido quimicamente , Animais , Cateninas/genética , Proliferação de Células , Quimiocinas , Modelos Animais de Doenças , Peptídeos e Proteínas de Sinalização Intercelular/genética , Masculino , MicroRNAs/genética , Ratos , Ratos Sprague-Dawley
7.
Zhongguo Zhong Yao Za Zhi ; 43(13): 2784-2788, 2018 Jul.
Artigo em Chinês | MEDLINE | ID: mdl-30111032

RESUMO

To study the effect of serum containing Xihuang pill on the proliferation of human breast cancer cell lines MDA-MB-435 and MCF-7 and the gene and protein expressions of Bcl-2, Bax, TP53, in order to explore the effect and mechanism of Xihuang pill in resisting breast cancer. The serum of the rats was prepared by the method of MTT assay. The expressions of Bcl-2 and Bax were detected by RT-PCR. The serum levels of Bcl-2 and Bax and the mRNA expression of TP53 were detected by immunofluorescence. The rats with serum containing Xihuang pill could inhibit the proliferation of MDA-MB-435 cells and MCF-7 cells (P<0.05). The serum containing Xihuang pill increased TP53 and Bax in MDA-MB-435 cells (P<0.05), and the ratio of Bcl-2/Bax was decreased (P<0.05). Meanwhile, the serum containing Xihuang pill could up-regulate the mRNA expression of Bax in MCF-7 cells and decrease the expression of Bcl (P<0.05), but there was no significant difference between the expression of TP53mRNA and Bax protein expressions after the treatment of MCF-7 cells with Xihuang pill serum. Serum containing Xihuang pill can induce the apoptosis of human breast cancer cells, and the mechanism of estrogen receptor-negative breast cancer cell apoptosis may be induced by up-regulating the mRNA expression of TP53, which can induce the expression of Bax and promote the metastasis of Bax to mitochondria, and ultimately play the role of inducing apoptosis.


Assuntos
Apoptose , Neoplasias da Mama , Animais , Proliferação de Células , Medicamentos de Ervas Chinesas , Humanos , Células MCF-7 , Ratos , Proteína X Associada a bcl-2
8.
Biomed Pharmacother ; 106: 976-982, 2018 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-30119269

RESUMO

Oxidative stress, inflammation, and hyperglycemia are considered to play crucial roles in the pathogenesis and progression of diabetic nephropathy (DN). Liquiritigenin, one of the flavonoid compounds, has been shown to possess anti-inflammatory, anti-hyperlipidemic, and anti-oxidative properties. Our study aimed to explore the effects of liquiritigenin on high glucose (HG)-induced extracellular matrix (ECM) accumulation, oxidative stress and inflammatory response and delineate the underlying mechanism. In our study, glomerular mesangial cells (HBZY-1) were co-treated with various doses of liquiritigenin and HG. We found that HG, but not normal glucose or mannitol, promoted the proliferation of HBZY-1 cells, which was suppressed by liquiritigenin. Liquiritigenin inhibited HG-induced ECM accumulation in HBZY-1 cells by reducing the expressions and production of collagen IV (Col IV) and fibronectin (FN). Moreover, liquiritigenin attenuated HG-induced oxidative stress, as evidenced by the decreased MDA content and NADPH oxidase 4 (NOX4) expression, and the increased SOD activity in HBZY-1 cells. Liquiritigenin suppressed HG-induced inflammatory response, as demonstrated by the reduced expressions and secretion of interleukin (IL)-6 and IL-1ß in HBZY-1 cells. Furthermore, we found that liquiritigenin inhibited HG-induced activation the nuclear factor-kappa B (NF-κB) and nod-like receptor protein 3 (NLRP3) inflammasome pathways. In conclusion, these results demonstrated that liquiritigenin attenuated HG-induced ECM accumulation, oxidative stress, and inflammation by suppression of the NF-κB and NLRP3 inflammasome pathways, suggesting that liquiritigenin might be a promising therapeutic agent for preventing the development of DN.


Assuntos
Anti-Inflamatórios/farmacologia , Antioxidantes/farmacologia , Nefropatias Diabéticas/prevenção & controle , Matriz Extracelular/efeitos dos fármacos , Flavanonas/farmacologia , Glomerulonefrite/prevenção & controle , Glucose/toxicidade , Inflamassomos/efeitos dos fármacos , Mediadores da Inflamação/metabolismo , Células Mesangiais/efeitos dos fármacos , NF-kappa B/metabolismo , Proteína 3 que Contém Domínio de Pirina da Família NLR/metabolismo , Estresse Oxidativo/efeitos dos fármacos , Animais , Linhagem Celular , Proliferação de Células/efeitos dos fármacos , Citoproteção , Nefropatias Diabéticas/imunologia , Nefropatias Diabéticas/metabolismo , Nefropatias Diabéticas/patologia , Relação Dose-Resposta a Droga , Matriz Extracelular/metabolismo , Matriz Extracelular/patologia , Glomerulonefrite/imunologia , Glomerulonefrite/metabolismo , Glomerulonefrite/patologia , Inflamassomos/imunologia , Inflamassomos/metabolismo , Células Mesangiais/imunologia , Células Mesangiais/metabolismo , Células Mesangiais/patologia , Ratos , Transdução de Sinais/efeitos dos fármacos
9.
Biomed Pharmacother ; 106: 1175-1181, 2018 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-30119185

RESUMO

Diabetic nephropathy (DN) is the leading cause of end-stage renal disease. It has been found that astilbin, a flavonoid compound, exerts a protective effect on DN. However, the role of astilbin in autophagy during DN is unknown. The human proximal tubular epithelial cells (HK-2 cells) were treated with high glucose (HG, 30 mM) in the presence or absence of astilbin. Cell viability was measured by MTT assay. The autophagy was determined by detecting the expression of LC3-II and p62 using western blot. The cell apoptosis was evaluated by detecting the apoptosis rate, caspase-3 activity, and the expression of Bcl-2 and Bax. The expression levels of protein kinase B (Akt) and p-Akt were detected by western blot. To determine whether the phosphatidylinositol-3-kinase (PI3K)/Akt pathway was involved in the effect of astilbin, cells were treated with the inhibitor of Akt, LY294002. We found that astilbin (10 and 20 µM) did not affect the viability of HK-2 cells, but attenuated HG-induced cell viability. Astilbin attenuated HG-induced autophagy and apoptosis in HK-2 cells. The expression of p-Akt was inhibited by HG treatment, while the inhibitory effect of HG was attenuated by astilbin. Inhibition of the PI3K/Akt signaling resisted the effect of astilbin on HG-induced apoptosis and autophagy. In conclusion, astilbin attenuated HG-induced autophagy and apoptosis in HK-2 cells through the PI3K/Akt pathway. The results indicated that astilbin might be a new therapeutic agent and be useful for improving clinical management of DN.


Assuntos
Apoptose/efeitos dos fármacos , Autofagia/efeitos dos fármacos , Nefropatias Diabéticas/prevenção & controle , Células Epiteliais/efeitos dos fármacos , Flavonóis/farmacologia , Glucose/toxicidade , Túbulos Renais Proximais/efeitos dos fármacos , Fosfatidilinositol 3-Quinase/metabolismo , Proteínas Proto-Oncogênicas c-akt/metabolismo , Proteínas Reguladoras de Apoptose/metabolismo , Proteínas Relacionadas à Autofagia/metabolismo , Linhagem Celular , Sobrevivência Celular/efeitos dos fármacos , Citoproteção , Nefropatias Diabéticas/enzimologia , Nefropatias Diabéticas/patologia , Relação Dose-Resposta a Droga , Células Epiteliais/enzimologia , Células Epiteliais/patologia , Humanos , Túbulos Renais Proximais/enzimologia , Túbulos Renais Proximais/patologia , Transdução de Sinais/efeitos dos fármacos
10.
Biomed Pharmacother ; 102: 1077-1083, 2018 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-29710524

RESUMO

Tangeretin (5, 6, 7, 8, 4'-pentamethoxyflavone), a natural compound extracted from citrus plants, has been shown to possess a variety of pharmacological activities, including anti-oxidant, anti-tumor, cytostatic and anti-diabetic properties. However, the role of tangeretin in diabetic nephropathy (DN) has not yet been investigated. This study was undertaken to elucidate the effects of tangeretin on high glucose (HG)-induced oxidative stress and extracellular matrix (ECM) accumulation in human glomerular mesangial cells (MCs) and explore the underlying mechanisms. Our results showed that tangeretin significantly inhibited HG-induced the proliferation of MCs. In addition, tangeretin dramatically reduced the levels of reactive oxygen species (ROS) and malondialdhyde (MDA), and induced SOD activity, as well as inhibited the expression of fibronectin (FN) and collagen IV in HG-stimulated MCs. Furthermore, tangeretin efficiently prevented the activation of ERK signaling pathway in HG-stimulated MCs. Taken together, these data indicated that tangeretin inhibits HG-induced cell proliferation, oxidative stress and ECM expression in glomerular MCs, at least in part, through the inactivation of ERK signaling pathway. Therefore, tangeretin may be a potential agent in the treatment of DN.


Assuntos
Matriz Extracelular/metabolismo , Flavonas/farmacologia , Glucose/toxicidade , Células Mesangiais/patologia , Ciclo Celular/efeitos dos fármacos , Ciclo Celular/genética , Linhagem Celular , Proliferação de Células/efeitos dos fármacos , Colágeno Tipo IV/metabolismo , Ativação Enzimática/efeitos dos fármacos , Matriz Extracelular/efeitos dos fármacos , Fibronectinas/metabolismo , Regulação da Expressão Gênica/efeitos dos fármacos , Humanos , Sistema de Sinalização das MAP Quinases/efeitos dos fármacos , Malondialdeído/metabolismo , Células Mesangiais/efeitos dos fármacos , Células Mesangiais/enzimologia , Células Mesangiais/metabolismo , NADPH Oxidases/metabolismo , Espécies Reativas de Oxigênio/metabolismo , Superóxido Dismutase/metabolismo , Fator de Crescimento Transformador beta1/metabolismo
11.
Dis Model Mech ; 11(3)2018 03 28.
Artigo em Inglês | MEDLINE | ID: mdl-29590639

RESUMO

Neutrophils are fast-moving cells essential for host immune functions. Although they primarily rely on glycolysis for ATP, isolated primary human neutrophils depend on mitochondrial membrane potential for chemotaxis. However, it is not known whether mitochondria regulate neutrophil motility in vivo, and the underlying molecular mechanisms remain obscure. Here, we visualized mitochondria in an interconnected network that localizes to the front and rear of migrating neutrophils using a novel transgenic zebrafish line. To disrupt mitochondrial function genetically, we established a gateway system harboring the CRISPR/Cas9 elements for tissue-specific knockout. In a transgenic line, neutrophil-specific disruption of mitochondrial DNA polymerase, polg, significantly reduced the velocity of neutrophil interstitial migration. In addition, inhibiting the mitochondrial electron transport chain or the enzymes that reduce mitochondrial reactive oxygen species also inhibited neutrophil motility. The reduced cell motility that resulted from neutrophil-specific knockout of sod1 was rescued with sod1 mRNA overexpression, or by treating with scavengers of reactive oxygen species. Together, our work has provided the first in vivo evidence that mitochondria regulate neutrophil motility, as well as tools for the functional characterization of mitochondria-related genes in neutrophils and insights into immune deficiency seen in patients with primary mitochondrial disorders.This article has an associated First Person interview with the first author of the paper.


Assuntos
Técnicas de Inativação de Genes , Mitocôndrias/metabolismo , Neutrófilos/metabolismo , Peixe-Zebra/metabolismo , Animais , Sequência de Bases , Movimento Celular , Clonagem Molecular , DNA Polimerase Dirigida por DNA/genética , Transporte de Elétrons , Dinâmica Mitocondrial , Especificidade de Órgãos , Oxirredução
12.
Cell Rep ; 22(7): 1810-1823, 2018 02 13.
Artigo em Inglês | MEDLINE | ID: mdl-29444433

RESUMO

MicroRNA-223 is known as a myeloid-enriched anti-inflammatory microRNA that is dysregulated in numerous inflammatory conditions. Here, we report that neutrophilic inflammation (wound response) is augmented in miR-223-deficient zebrafish, due primarily to elevated activation of the canonical nuclear factor κB (NF-κB) pathway. NF-κB over-activation is restricted to the basal layer of the surface epithelium, although miR-223 is detected throughout the epithelium and in phagocytes. Not only phagocytes but also epithelial cells are involved in miR-223-mediated regulation of neutrophils' wound response and NF-κB activation. Cul1a/b, Traf6, and Tab1 are identified as direct targets of miR-223, and their levels rise in injured epithelium lacking miR-223. In addition, miR-223 is expressed in cultured human bronchial epithelial cells, where it also downregulates NF-κB signaling. Together, this direct connection between miR-223 and the canonical NF-κB pathway provides a mechanistic understanding of the multifaceted role of miR-223 and highlights the relevance of epithelial cells in dampening neutrophil activation.


Assuntos
Inflamação/patologia , Queratinócitos/metabolismo , MicroRNAs/metabolismo , NF-kappa B/metabolismo , Neutrófilos/patologia , Transdução de Sinais , Nadadeiras de Animais/fisiologia , Animais , Sequência de Bases , Brônquios/citologia , Embrião não Mamífero/metabolismo , Células Epiteliais/metabolismo , Células HEK293 , Humanos , Inflamação/metabolismo , MicroRNAs/genética , Neutrófilos/metabolismo , Fagócitos/metabolismo , Regeneração , Peixe-Zebra/embriologia , Peixe-Zebra/genética , Proteínas de Peixe-Zebra/metabolismo
13.
Biol. Res ; 51: 31, 2018. graf
Artigo em Inglês | LILACS-Express | ID: biblio-983936

RESUMO

Abstract Background: miR-214 was demonstrated to be upregulated in models of renal disease and promoted fibrosis in renal injury independent of TGF-β signaling in vivo. However, the detailed role of miR-214 in acute kidney injury (AKI) and its underlying mechanism are still largely unknown. Methods: In this study, an I/R-induced rat AKI model and a hypoxia-induced NRK-52E cell model were used to study AKI. The concentrations of kidney injury markers serum creatinine, blood urea nitrogen, and kidney injury molecule-1 were measured. The expressions of miR-214, tumor necrosis factor-α, interleukin (Ε)-1β, IL-6, were detected by RT-qPCR. The protein levels of Bcl-2, Bax, Dickkopf-related protein 3, β-catenin, c-myc, and cyclinD1 were determined by western blot. Cell apoptosis and caspase 3 activity were evaluated by flow cytometry analysis and caspase 3 activity assay, respectively. Luciferase reporter assay was used to confirm the interaction between miR-214 and Dkk3. Results: miR-214 expression was induced in ischemia-reperfusion (I/R)-induced AKI rat and hypoxic incubation of NRK-52E cells. Overexpression of miR-214 alleviated hypoxia-induced NRK-52E cell apoptosis while inhibition of miR-214 expression exerted the opposite effect. Dkk3 was identified as a target of miR-214. Anti-miR-214 abolished the inhibitory effects of DKK3 knockdown on hypoxia-induced NRK-52E cell apoptosis by inactivation of Wnt/β-catenin signaling. Moreover, miR-214 ameliorated AKI in vivo by inhibiting apoptosis and fibrosis through targeting Dkk3 and activating Wnt/β -catenin pathway. Conclusion: miR-214 ameliorates AKI by inhibiting apoptosis through targeting Dkk3 and activating Wnt/β -catenin signaling pathway, offering the possibility of miR-214 in the therapy of ischemic AKI.

14.
Biomed Pharmacother ; 96: 471-479, 2017 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-29031207

RESUMO

Diabetic nephropathy (DN) has become the major cause of end-stage renal disease (ESRD). It has been demonstrated that apoptosis of renal tubular epithelial cells induced by hyperglycemia contributes to the pathogenesis of DN. Recent researches have corroborated the critical roles of microRNAs (miRNAs) in the apoptosis of various types of cells including renal tubular epithelial cells. However, the eff ; ;ect of miRNAs on the hyperglycemia-induced apoptosis of renal tubular epithelial cells remains unclear. The aim of this study is to explore the eff ; ;ect of miRNAs on the hyperglycemia-induced apoptosis of renal tubular epithelial cells and its molecular mechanism. Using a miRNA microarray, miRNAs putatively associated with DN were examined in renal biopsy tissue samples from DN patients and healthy controls. Validation analysis of miR-25 level in serum samples and renal biopsy tissue samples was performed using quantitative reverse transcription PCR (qRT-PCR). Then, gain- and loss- of function experiments were performed to determine the protective roles of miR-25 in high glucose-induced damage to renal tubular epithelial cells. Furthermore, the target gene of miR-25 and the downstream signaling pathway were also investigated. Microarray analysis and qRT-PCR revealed that miR-25 was significantly downregulated in renal biopsy tissue and serum samples from DN patients. We also observed that an inverse relationship between serum miR-25 level and proteinuria in DN patients. Meanwhile, miR-25 was decreased in human kidney (HK-2) cells subjected to HG treatment in a time dependent manner. Its overexpression reduced production of reactive oxygen species (ROS), suppressed cell apoptosis in HG-induced cell damage model, which was coupled with the decreased expression of cleaved caspase-3 and activity of caspase-3. Subsequent analyses demonstrated that phosphatase and tensin homolog deleted on chromosome ten (PTEN) was a direct and functional target of miR-25, which was validated by the dual luciferase reporter assay. Most importantly, the overexpression of PTEN effectively reversed the protective effects of miR-25 mimics on renal tubular epithelial cell injury. We also found that the anti-apoptotic effects of miR-25 are dependent on the activation of PTEN/Akt pathway. In addition, we observed that PTEN was upregulated in renal biopsy tissue samples from patients with DN, and an inverse relationship was found between PTEN and miR-25 expression, suggesting that miR-25 may exert its function through regulation of PTEN in DN. Taken together, our study proved that overexpression of miR-25 could ameliorate HG-induced oxidative stress and apoptosis in renal tubular epithelial cells through activation of PTEN/AKT pathway, suggesting that overexpression of miR-25 might provide a potential therapeutic approach for DN.


Assuntos
Células Epiteliais/metabolismo , Glucose/toxicidade , Túbulos Renais/metabolismo , MicroRNAs/biossíntese , PTEN Fosfo-Hidrolase/metabolismo , Proteínas Proto-Oncogênicas c-akt/metabolismo , Adulto , Apoptose/efeitos dos fármacos , Apoptose/fisiologia , Diabetes Mellitus Tipo 2/sangue , Células Epiteliais/efeitos dos fármacos , Feminino , Humanos , Túbulos Renais/efeitos dos fármacos , Masculino , MicroRNAs/sangue , Pessoa de Meia-Idade , Transdução de Sinais/efeitos dos fármacos , Transdução de Sinais/fisiologia
15.
Dis Model Mech ; 10(11): 1323-1332, 2017 11 01.
Artigo em Inglês | MEDLINE | ID: mdl-28954734

RESUMO

Neutrophilic inflammation is essential for defending against invading pathogens, but can also be detrimental in many clinical settings. The hematopoietic-specific small Rho-GTPase Rac2 regulates multiple pathways that are essential for neutrophil activation, including adhesion, migration, degranulation and production of reactive oxygen species. This study tested the hypothesis that partially suppressing rac2 in zebrafish neutrophils by using a microRNA (miRNA) would inhibit neutrophil migration and activation, which would reduce the immunological damage caused by systemic inflammation. We have generated a transgenic zebrafish line that overexpresses microRNA-722 (miR-722) in neutrophils. Neutrophil motility and chemotaxis to tissue injury or infection are significantly reduced in this line. miR-722 downregulates the transcript level of rac2 through binding to seed-matching sequence in the rac2 3'UTR. Furthermore, miR-722-overexpressing larvae display improved outcomes in both sterile and bacterial systemic models, which correlates with a robust upregulation of the anti-inflammatory cytokines in the whole larvae and isolated neutrophils. Finally, an miR-722 mimic protects zebrafish from lethal lipopolysaccharide challenge. Together, these results provide evidence for and the mechanism of an anti-inflammatory miRNA that restrains detrimental systemic inflammation.


Assuntos
Inflamação/genética , MicroRNAs/metabolismo , Neutrófilos/metabolismo , Neutrófilos/patologia , Proteínas de Peixe-Zebra/metabolismo , Peixe-Zebra/genética , Proteínas rac de Ligação ao GTP/metabolismo , Regiões 3' não Traduzidas/genética , Animais , Animais Geneticamente Modificados , Sequência de Bases , Quimiotaxia/genética , Regulação para Baixo/genética , Larva/genética , Lipopolissacarídeos , MicroRNAs/genética , Fenótipo , Ligação Proteica , Proteínas de Peixe-Zebra/genética , Proteínas rac de Ligação ao GTP/genética
16.
Dalton Trans ; 46(19): 6358-6365, 2017 May 16.
Artigo em Inglês | MEDLINE | ID: mdl-28463366

RESUMO

We report a fast and simple method for the synthesis of Ni-based metal-organic-frameworks (Ni-MOFs). Due to the existence of nickel ions and an organic ligand, the MOFs are employed as a sacrificial template for the facile preparation of carbon-embedded Ni (Ni/C) catalysts by a direct thermal decomposition method. The obtained Ni/C catalysts exhibit excellent catalytic activity for selectively transforming furfural (FAL) to tetrahydrofurfuryl alcohol (THFOL) due to the Ni nanoparticles (NPs) embedded uniformly in the ligand-derived carbon. The exemplified results illustrate that the catalytic performance of the Ni/C catalyst is greatly affected by the calcination conditions (temperature and time), composition of the Ni-MOF precursor and the catalysis conditions. The conversion of FAL and selectivity of THFOL both reached 100% under the conditions of 120 °C, 1 MPa H2 pressure and 120 min of hydrogenation over the Ni/C-500 catalyst, derived from the pyrolysis of Ni-MOFs (Ni : BTC mole ratio of 1.0) at 500 °C for 120 min, which exhibits an average nanoparticle size of ∼14 nm and uniform dispersion, and the highest BET surface area (∼92 m2 g-1) among all investigated Ni/C catalysts. This facilely prepared heterogeneous catalyst would be very promising for the replacement of noble metal catalysts for the efficient catalytic conversion of biomass-derived feedstocks into value-added chemicals.

17.
Oncol Lett ; 13(2): 857-866, 2017 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-28356970

RESUMO

Gap junctions (GJs) serve the principal role in the antineoplastic (cytotoxicity and induced apoptosis) effect of chemical drugs. The aim of the present study was to determine the effect of GJ intercellular communication (GJIC) composed of connexin 43 (Cx43) on adriamycin cytotoxicity in breast cancer cells. Four cell lines (Hs578T, MCF-7, MDA-MB-231 and SK-BR-3) with different degree of malignancy were used in the study. The results of western blotting and immunofluorescence revealed that, in Hs578T and MCF-7 cells, which have a low degree of malignancy, the expression levels of Cx43 and GJIC were higher than those in MDA-MB-231 and SK-BR-3 cells (which have a high degree of malignancy). In Hs578T and MCF-7 cells, where GJ could be formed, the function of GJ was modulated by a pharmacological potentiators [retinoid acid (RA)]/inhibitors [oleamide and 18-α-glycyrrhetinic acid (18-α-GA)] and small interfering RNA (siRNA). In high-density cells (where GJ was formed), enhancement of GJ function by RA increased the cytotoxicity of adriamycin, while inhibition of GJ function by oleamide/18-α-GA and siRNA decreased the cytotoxicity caused by adriamycin. Notably, the modulation of GJ did not affect the survival of cells treated with adriamycin when cells were in low density (no GJ was formed). The present study illustrated the association between GJIC and the antitumor effect of adriamycin in breast cancer cells. The cytotoxicity of adriamycin on breast cancer cells was increased when the function of gap junctions was enhanced.

18.
Chemphyschem ; 18(9): 1146-1154, 2017 May 05.
Artigo em Inglês | MEDLINE | ID: mdl-28125162

RESUMO

A simple synthetic route is presented for fabricating gold nanoparticle (NP)-decorated bismuth oxychloride (BiOCl) nanosheets in one step based on laser ablation of a gold target in a hydrochloric acid solution of bismuth nitrate without surfactant. After laser ablation, BiOCl nanosheets with attached Au NPs are obtained. The nanosheets are sub-micron in the planar dimension and around 20 nm thick, and the Au NPs are a mean size of approximately 20 nm. Further experiments reveal that such Au-NP-decorated nanosheets could be formed at a large Cl/Bi molar ratio range (0.01 to 3) in solution. The formation of the BiOCl nanosheets is attributed to the Au plasma plume-induced local fast hydrothermal reaction, which drives the planar growth of BiOCl. Importantly, these Au-NP-decorated BiOCl nanosheets exhibit high photodegradation activity on rhodamine B, a typical organic pollutant, compared with bare nanosheets under visible light irradiation, and show highly stable and recyclable performance. This is attributed to the plasmonic properties of Au NPs, which increase optical absorption and promote separation of electron-hole pairs in the NP-decorated BiOCl nanosheets. This work provides not only a new plasmonic photocatalyst for the oxidative degradation of organic pollutants, but also a general method for fabrication of the metal-NP-decorated nanosheets of other layer-structured oxychlorides.

19.
ACS Appl Mater Interfaces ; 9(7): 6615-6623, 2017 Feb 22.
Artigo em Inglês | MEDLINE | ID: mdl-28135064

RESUMO

An interface stabilizer based on alkylation-functionalized fullerene derivatives, [6, 6]-Phenyl-C61-butyric acid (3,5-bis(octyloxy)phenyl)methyl ester (PCB-C8oc), was successfully synthesized and applied for the active layer of Organic Photovoltaics (OPVs). The PCB-C8oc can replace part of the phenyl-C61-buty-ric acid methyl ester (PCBM) and be distributed on the interface of poly(3-hexylthiophene) (P3HT) and PCBM to form P3HT/PCBM/PCB-C8oc ternary blends, leading to thermally stable and efficient organic photovoltaics. The octyl groups of PCB-C8oc exhibit intermolecular interaction with the hexyl groups of P3HT, and the fullerene unit of PCB-C8oc are in tight contact with PCBM. The dual functions of PCB-C8oc will inhibit the phase separation between electron donor and acceptor, thereby improving the stability of devices under long-time thermal annealing at high temperature. When doped with 10 wt % PCB-C8oc, the power conversion efficiency (PCE) of the P3HT system decreased from 3.54% to 2.88% after 48 h of thermal treatment at 150 °C, whereas the PCE of the reference device without PCB-C8oc dramatically dropped from 3.53% to 0.73%. When doping 10 or 20 wt % PCB-C8oc, the unannealed P3HT/PCBM/PCB-C8oc device achieved a higher PCE than the P3HT/PCBM device without any annealing following the same fabricating condition. For the PTB7/PCBM-based devices, after adding only 5 wt % PCB-C8oc, the OPVs also exhibited thermally stable morphology and better device performances. All these results demonstrate that the utilization of alkyl interchain interactions is an effective and practical strategy to control morphological evolution.

20.
Chemphyschem ; 18(9): 1133-1139, 2017 May 05.
Artigo em Inglês | MEDLINE | ID: mdl-28097772

RESUMO

Laser melting in liquids (LML) is one of the most effective methods to prepare bimetallic alloys; however, despite being an ongoing focus of research, the process involved in the formation of such species remains ambiguous. In this paper, we prepared two types of Pt-based bimetallic alloys by LML, including Pt-Au alloys and Pt-iron group metal (iM=Fe/Co/Ni) alloys, and investigated the corresponding mechanisms of alloying process. Detailed component and structural characterizations indicate that laser irradiation induced a quite rapid formation process (not exceeding 10 s) of Pt-Au alloy nanospheres, and the crystalline structures of Pt-Au alloys is determined by the monometallic constituents with higher content. For Pt-iM alloys, we provide direct evidence to support the conclusion that FeOx /CoOx /NiOx colloids can be reduced to elementary Fe/Co/Ni particles by ethanol molecules during laser irradiation, which then react with Pt colloids to form Pt-iM sub-microspheres. These results demonstrate that LML provides an optional route to prepare Pt-based bimetallic alloy particles with tunable size, components, and crystalline phase, which should have promising applications in biological and catalysis studies.

SELEÇÃO DE REFERÊNCIAS
DETALHE DA PESQUISA