RESUMEN
The development of photocatalysts with a wide spectral response and effective carrier separation capability is essential for the green degradation of tetracycline hydrochloride. In this study, a magnetic recyclable Z-scheme ZnO/ZnFe2O4 heterojunction (ZZF) was successfully constructed via the solid phase method, using MIL-88A(Fe)@Zn as the precursor. An appropriate band gap width and Z-scheme charge transfer mechanism provide ZZF with excellent visible light absorption performance, efficient charge separation, and a strong redox ability. Under visible light irradiation, the degradation efficiency of tetracycline hydrochloride for the optimal sample can reach 86.3% within 75 min in deionized water and 92.9% within 60 min in tap water, exhibiting superior stability and reusability after five cycles. Moreover, the catalyst in the water can be conveniently recovered by magnetic force. After visible light irradiation for 70 min, the temperature of the reaction system increased by 21.9 °C. Its degradation constant (35.53 × 10-3 min-1) increased to 5.1 times that at room temperature (6.95 × 10-3 min-1). Using thermal energy enhances the kinetic driving force of the reactants and facilitates carrier migration, meaning that more charge is available for the production of â¢O2- and â¢OH. This study provides a potential candidate for the efficient degradation of tetracycline hydrochloride by combining thermal catalysis with a photocatalytic heterojunction.
RESUMEN
The build-in electric field by the construction of heterojunction is one of the most promising strategies to suppress the recombination of photogenerated carriers. Here, we reported a piezo-photocatalytic system composed of Se-decorated CdS nanowires and few-layered edge-on MoSe2 nanosheets for efficient H2 generation by two-pot hydrothermal synthesis. The few-layered MoSe2 exposed abundant edge sites for hydrogen evolution reaction (HER). The activity of 20-MoSe2/CdS0.95Se0.05 (20-MS/CSS, with 20 mol% of MoSe2 loading) nanocomposite casted a remarkable photocatalytic HER performance, with a rate of 47.3 mmol h-1 g-1. Moreover, MoSe2 nanosheets deformed to generate the piezoelectric polarization field under magnetic stirring, which rendered efficient separation of photogenerated carriers, resulting in a piezo-photocatalytic synergistic effect. As a result, the HER of 20-MS/CSS at 900 rpm for piezo-photocatalysis was 59.1 mmol h-1 g-1, which was 1.25 times that of 20-MS/CSS for photocatalysis. Meanwhile, the photoelectrochemical measurements further visualized the piezo-photoelectric synergy. This study exposes a new way for utilizing mechanical energy to improve photocatalytic performance, and achieving high piezo-photocatalysis.
Asunto(s)
Hidrógeno , Nanocables , Hidrógeno/química , Sulfuros/química , Procesos Fotoquímicos , CatálisisRESUMEN
Nano-semiconductor materials coupled with piezoelectric effect have received extensive attention due to their wide application in catalysis. In this work, few-layered MoSe2 nanosheets were grown vertically on TiO2 nanorods (TNr) to synthesize a direct Z-scheme heterojunction, exhibiting efficient piezocatalytic and piezo-photocatalytic performance. The MoSe2/TNr heterostructure exhibited superior piezoelectric degradation efficiency, successfully removing over 98% of RhB within 360 s under continuous magnetic stirring in dark. Compared with piezocatalysis, the piezo-photocatalytic system possessed higher degradation efficiency and cycle stability. Furthermore, a piezo-photoelectric synergistic effect of nanocomposites was observed by current outputs. Under stirring conditions, the current density of depleted MoSe2/TNr and MoSe2 nanosheets were respectively 6.3 µA/cm2 and 5.5 µA/cm2. When light and stirring were applied, the MoSe2/TNr current density increased twice to 13.2 µA/cm2, while the MoSe2 nanosheets didn't exhibit improvement. Through the direct Z-scheme heterojunction of MoSe2/TNr, photoexcitation and piezoelectric polarization work together to effectively replenish carriers under light irradiation, and then rapidly separate free charges through piezopotential. This work broadens the application prospects of piezocatalysis and piezo-photocatalysis in renewable energy harvesting and water purification.
RESUMEN
In this work, hierarchical core-shell NiMoO4@Ni-Co-S nanorods were first successfully grown on nickel foam by a facile two-step method to fabricate a bind-free electrode. The well-aligned electrode wrapped by Ni-Co-S nanosheets displays excellent nanostructural properties and outstanding electrochemical performance, owing to the synergistic effects of both nickel molybdenum oxides and nickel cobalt sulfides. The prepared core-shell nanorods in a three-electrode cell yielded a high specific capacitance of 2.27 F cm-2 (1892 F g-1) at a current density of 5 mA cm-2 and retained 91.7% of the specific capacitance even after 6000 cycles. Their electrochemical performance was further investigated for their use as positive electrode for asymmetric supercapacitors. Notably, the energy density of the asymmetric supercapacitor device reached 2.45 mWh cm-3 at a power density of 0.131 W cm-3, and still retained a remarkable 80.3% of the specific capacitance after 3500 cycles. There is great potential for the electrode composed of the core-shell NiMoO4@Ni-Co-S nanorods for use in an all-solid-state asymmetric supercapacitor device.
RESUMEN
The HOXB1 gene plays a critical role as an oncogene in diverse tumors. However, the functional role of HOXB1 and the mechanism regulating HOXB1 expression in glioma are not fully understood. A preliminary bioinformatics analysis showed that HOXB1 is ectopically expressed in glioma, and that HOXB1 is a possible target of miR-3175. In this study, we investigated the function of HOXB1 and the relationship between HOXB1 and miR-3175 in glioma. We show that HOXB1 expression is significantly downregulated in glioma tissues and cell lines, and that its expression may be closely associated with the degree of malignancy. Reduced HOXB1 expression promoted the proliferation and invasion of glioma cells, and inhibited their apoptosis in vitro, and the downregulation of HOXB1 was also associated with worse survival in glioma patients. More importantly, HOXB1 was shown experimentally to be a direct target of miR-3175 in this study. The downregulated expression of miR-3175 inhibited cell proliferation and invasion, and promoted apoptosis in glioma. The oncogenicity induced by low HOXB1 expression was prevented by an miR-3175 inhibitor in glioma cells. Our results suggest that HOXB1 functions as a tumor suppressor, regulated by miR-3175 in glioma. These results clarify the pathogenesis of glioma and offer a potential target for its treatment.
Asunto(s)
Neoplasias Encefálicas/genética , Regulación Neoplásica de la Expresión Génica , Genes Supresores de Tumor , Glioma/genética , Proteínas de Homeodominio/genética , MicroARNs/genética , Apoptosis , Encéfalo/metabolismo , Encéfalo/patología , Neoplasias Encefálicas/diagnóstico , Neoplasias Encefálicas/patología , Línea Celular Tumoral , Proliferación Celular , Glioma/diagnóstico , Glioma/patología , Humanos , Invasividad Neoplásica/diagnóstico , Invasividad Neoplásica/genética , Invasividad Neoplásica/patología , Pronóstico , Interferencia de ARN , ARN Interferente Pequeño/genéticaRESUMEN
Although paclitaxel is an effective chemotherapeutic drug used in the treatment of many tumors, hepatoma cells, in particular, are known to be highly resistant to it. Previously, we discovered that Lin28 was closely associated with resistance to paclitaxel in Hep3B cells. The nuclear factor-kappa B (NF-κB) transcription factor, which plays an important role in tumor survival, directly activates Lin28 expression through a binding site on the first intron. Curcumin, a non-toxic anti-inflammatory agent, inhibits NF-κB activity in vitro. In this study, we reported that a combination of curcumin and paclitaxel exhibited synergistic anti-proliferative and pro-apoptosis effects on Hep3B cells, and curcumin down-regulated paclitaxel-induced enhanced expression of Lin28 and NF-κB activation. Furthermore, our results revealed that curcumin reduced Lin28 levels via mechanisms directly mediated by inhibition of NF-κB activity. These mechanism-based observations evidence that curcumin enhances the sensitivity of hepatoma cells to paclitaxe, and strongly support the notion that paclitaxel in combination with curcumin may provide a superior therapeutic index for HCC chemotherapy.
Asunto(s)
Protocolos de Quimioterapia Combinada Antineoplásica/farmacología , Carcinoma Hepatocelular/metabolismo , Resistencia a Antineoplásicos/efectos de los fármacos , Regulación Neoplásica de la Expresión Génica/efectos de los fármacos , Neoplasias Hepáticas/metabolismo , FN-kappa B/metabolismo , Proteínas de Unión al ARN/metabolismo , Apoptosis/efectos de los fármacos , Western Blotting , Carcinoma Hepatocelular/tratamiento farmacológico , Carcinoma Hepatocelular/genética , Carcinoma Hepatocelular/patología , Proliferación Celular/efectos de los fármacos , Curcumina/administración & dosificación , Humanos , Neoplasias Hepáticas/tratamiento farmacológico , Neoplasias Hepáticas/genética , Neoplasias Hepáticas/patología , FN-kappa B/genética , Paclitaxel/administración & dosificación , ARN Mensajero/genética , Proteínas de Unión al ARN/genética , Reacción en Cadena en Tiempo Real de la Polimerasa , Reacción en Cadena de la Polimerasa de Transcriptasa Inversa , Células Tumorales CultivadasRESUMEN
Hepatocellular carcinoma (HCC) is highly resistant to chemotherapeutic drugs, which markedly reduces the effect of chemotherapy. Lin28 has been shown to contribute to tumor relapse after chemotherapy; however, the relationship between Lin28 and chemotherapy drug resistance is unknown. In the present study, we established a drug-resistant Hep3B cell line to investigate the association between Lin28 and drug resistance in HCC, and we identified the underlying mechanisms. We found that the expression of Lin28 was closely associated with resistance to paclitaxel. The drugresistant Hep3B cell line, which expresses high levels of Lin28, is more resistant to paclitaxel and other anticancer drugs than the parental cell line. Moreover, further studies showed that dysregulation of Lin28 inhibited let-7 family microRNA levels and upregulated the anti-apoptotic protein Bcl-xL, which is a target of let-7. Our results indicate that the Lin28/let-7/Bcl-xL pathway underlies the drug resistance of Hep3B cells.
Asunto(s)
Antineoplásicos/farmacología , Carcinoma Hepatocelular/genética , Resistencia a Antineoplásicos , Neoplasias Hepáticas/genética , Proteínas de Unión al ARN/genética , Proteína bcl-X/genética , Carcinoma Hepatocelular/tratamiento farmacológico , Línea Celular Tumoral , Cisplatino/farmacología , Ciclofosfamida/farmacología , Regulación Neoplásica de la Expresión Génica/efectos de los fármacos , Humanos , Neoplasias Hepáticas/tratamiento farmacológico , MicroARNs/genética , Paclitaxel/farmacología , Regulación hacia ArribaRESUMEN
There are two isoforms of apolipoprotein B (apoB) in mammals: apoB-100 and apoB-48. The latter is generated by C-to-U editing of apoB mRNA, catalyzed by the apolipoprotein B mRNA editing enzyme, namely, catalytic polypeptide 1 (APOBEC-1). Lipid particles containing apoB-48 are cleared from the plasma more rapidly than those containing apoB-100 and thus do not contribute to plaque formation in the arterial wall. In the present study, we analyzed whether curcumin is capable of regulating lipid metabolism by improving the level of apoB mRNA editing. The cytotoxicity of curcumin in hepatocytes was determined using the 3-(4,5-dimethylthiazol2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and the levels of APOBEC-1 mRNA and protein were analyzed by real-time quantitative polymerase chain reaction (qRT-PCR) and western blotting. The efficiency of apoB mRNA editing was determined by reverse transcription PCR (RT-PCR) products and cloning sequencing analysis. We demonstrated that curcumin concentrations up to 70 µM had no significant cytotoxic effects on primary rat hepatocytes at 24 h. At 15 µM, curcumin significantly increased the expression of APOBEC-1 mRNA and protein, and increased the editing level of apoB mRNA from 3.13 to 7.53%. At 25 µM, curcumin reduced the expression of APOBEC-1; however, it did not affect the apoB mRNA editing level. Our data suggested that curcumin at a concentration of 15 µM raised the level of apoB-48 and reduced the level of apoB-100 by increasing the expression of APOBEC-1 in primary rat hepatocytes; therefore, curcumin may be a novel preventative therapy for atherosclerosis.