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1.
Sci Total Environ ; 698: 134238, 2020 Jan 01.
Artigo em Inglês | MEDLINE | ID: mdl-31505360

RESUMO

Different biomass materials (walnut shell, coconut shell or cottonwood sawdust) were co-pyrolyzed with carbon-enriched oily sludge to produce aqueous phase sulfamethoxazole (SMZ) adsorption materials. The co-pyrolysis char was activated with K2CO3 to modify its micro-structure and functional groups. Results show that ACs prepared from the mixture contained more mesopores than biomass-based ACs, more porous and higher yield than oily sludge-based ACs. One-step activation method was more attractive than two-step activation in larger specific surface area (up to almost 4 times), wider pore size distribution (2-3 nm), stronger SMZ adsorption ability (higher than 2 times). The maximum BET surface area was 1342 m2/g for the ACs prepared from the mixture of walnut shell and oily sludge by one-step activation and it had the maximum SMZ adsorption capacity up to 361.9 mg/g, which is higher than previous reported values. The capacity of SMZ adsorption of ACs was mainly attributed to pore size distribution, specific surface area and functional groups. Among them, the appropriate content of CO and CO functional groups, larger specific area and more pores range from 2 to 3 nm lead to higher adsorption capacity.


Assuntos
Modelos Químicos , Sulfametoxazol/química , Adsorção , Biomassa , Carbono/química , Carvão Vegetal/química , Cinética , Óleos , Porosidade , Pirólise
2.
Biomed Pharmacother ; 116: 109007, 2019 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-31170663

RESUMO

It's critical for tube formation and angiogenesis to repair ischemic myocardium or stroke. This study aimed to investigate role of microRNA-126 (miR-126) in tube formation in human umbilical vein endothelial cells (HUVECs) and associated mechanisms. Primary neural stem cells (NSCs) and HUVECs were cultured and transfected with microRNA-126 mimics and miR-126 inhibitor. Cell counting kit-8 (CCK-8) and cell cycle assay were conducted for evaluating NSCs viability. Transwell assay was conducted to observe invasive ability of HUVECs. Quantitative real-time PCR (qRT-PCR) assay was used to examine epidermal growth factor like domain 7 (EGFL7) and miR-126 mRNA both in vitro and animal models. Tube forming capability was evaluated in HUVECs. Dual luciferase assay was performed to evaluate interaction between miR-126 and EGFL7 gene. Western blot assay was used to determine phosphoinositide-3-kinase/protein kinase-B (PI3K/AKT) signaling molecules and EGFL7. The results indicated that miR-126 significantly decreased cell viability, inhibited invasive ability and modulated cell cycle of NSCs compared to miR-NC group (p < 0.05). miR-126 significantly inhibited tube formation of HUVECs compared to miR-NC group (p < 0.05). miR-126 significantly down-regulated EGFL7 mRNA and protein expression compared to miR-NC (p < 0.05). Atorvastatin significantly increased CD34 and enhanced EGFL7 expression in traumatic brain injury (TBI) rats brain tissues compared to Model group (p < 0.05). miR-126 significantly down-regulated and atorvastatin up-regulated PI3K/AKT signaling pathway (p < 0.05). Atorvastatin significantly increased EGFL7 and down-regulated miR-126 expression in TBI rats brain tissues compared to Model group (p < 0.05). miR-126 interacted with and negatively correlated with EGFL7 gene both in vitro and in TBI models. In conclusion, microRNA-126 inhibited tube formation of HUVECs by interacting with EGFL7 and down-regulating PI3K/AKT signaling pathway.


Assuntos
Proteínas de Ligação ao Cálcio/metabolismo , Regulação para Baixo/genética , Família de Proteínas EGF/metabolismo , Células Endoteliais da Veia Umbilical Humana/metabolismo , MicroRNAs/metabolismo , Neovascularização Fisiológica , Fosfatidilinositol 3-Quinases/metabolismo , Proteínas Proto-Oncogênicas c-akt/metabolismo , Transdução de Sinais , Animais , Antígenos CD34/metabolismo , Atorvastatina/administração & dosagem , Atorvastatina/farmacologia , Sequência de Bases , Lesões Encefálicas Traumáticas/genética , Lesões Encefálicas Traumáticas/patologia , Proteínas de Ligação ao Cálcio/genética , Ciclo Celular/efeitos dos fármacos , Ciclo Celular/genética , Sobrevivência Celular/efeitos dos fármacos , Sobrevivência Celular/genética , Regulação para Baixo/efeitos dos fármacos , Família de Proteínas EGF/genética , Fatores de Crescimento Endotelial/metabolismo , Humanos , MicroRNAs/genética , Neovascularização Fisiológica/efeitos dos fármacos , Neovascularização Fisiológica/genética , Células-Tronco Neurais/efeitos dos fármacos , Células-Tronco Neurais/metabolismo , RNA Mensageiro/genética , RNA Mensageiro/metabolismo , Ratos Sprague-Dawley , Regulação para Cima/efeitos dos fármacos , Regulação para Cima/genética
3.
Int J Clin Exp Pathol ; 8(10): 12234-42, 2015.
Artigo em Inglês | MEDLINE | ID: mdl-26722408

RESUMO

OBJECTIVE: To investigate the role and mechanism of epidermal growth factor like domain 7 (EGFL7) in glioma angiogenesis by cell co-culture and RNA interference. METHODS: NSCs-HUVECs co-culture system was established using Transwell culturing techniques. The interactions between glioma and endothelial cells were simulated in-vitro. Cellular expression of EGFL7 in NSCs and HUVEC was targeted and suppressed by lentiviral vector carrying siRNA. The effect of EGFL7 on angiogenesis in glioma in-vitro micro-environment was detected by endothelial cell proliferation, adhesion and tube formation assay. RESULTS: Following EGFL7 gene silencing, expression of EGFL7 in HUVECs was reduced and cell adhesion capability was inhibited significantly. Endothelial cells failed to form a lumen-like structure after EGFL7 gene silencing, shown by the tube formation assay. CONCLUSION: By regulating endothelial cell adhesion, EGFL7 plays a key role in the regulation of glioma angiogenesis.


Assuntos
Fatores de Crescimento Endotelial/metabolismo , Glioma/patologia , Neovascularização Patológica/patologia , Proteínas de Ligação ao Cálcio , Adesão Celular , Proliferação de Células , Técnicas de Cocultura , Família de Proteínas EGF , Células Endoteliais/metabolismo , Células Endoteliais/patologia , Fatores de Crescimento Endotelial/genética , Glioma/metabolismo , Células-Tronco Embrionárias Humanas , Células Endoteliais da Veia Umbilical Humana , Humanos , Neovascularização Patológica/metabolismo , Interferência de RNA
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