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1.
J Nanosci Nanotechnol ; 20(2): 731-740, 2020 Feb 01.
Artigo em Inglês | MEDLINE | ID: mdl-31383068

RESUMO

NiO/ZnO gas-sensing nanotube materials were prepared by electrospinning. The structure and morphology of the samples were characterized by X-ray diffraction (XRD), scanning electron microscopy (SEM), transmission electron microscopy (TEM), X-ray photoelectron spectroscopy (XPS), energydispersive X-ray detection (EDX) and Brunauer-Emmett-Teller (BET) analysis. The template, PAN (peroxyacetyl nitrate) fibers, was completely removed, as evidenced by the EDX results. The final NiO/ZnO composite materials were composed of hexagonal wurtzite ZnO and cubic NiO and exhibited hollow tubular structures. In the composites, p-n heterojunctions were formed at the interface of NiO and ZnO. The results of gas sensitivity tests showed that the incorporation of NiO considerably improved the gas sensitivity of ZnO to ethanol. When the doping ratio was 0.125 mol/mol, the composites exhibited the highest sensitivity to ethanol (100.92 at 300 °C) and showed high selectivity.

2.
Chem Commun (Camb) ; 2018 Dec 07.
Artigo em Inglês | MEDLINE | ID: mdl-30525140

RESUMO

A homochiral open-framework fluorinated cobalt phosphate with a 2-fold interpenetrating diamond topology was ionothermally synthesized. The significant enantiomeric excess of the bulk product was confirmed by strong signals in its solid state circular dichroism (CD) spectrum.

3.
J Neurogastroenterol Motil ; 23(1): 117-123, 2017 Jan 30.
Artigo em Inglês | MEDLINE | ID: mdl-27436346

RESUMO

Background/Aims: Myenteric plexus interstitial cells of Cajal (ICC-MY) are involved in the generation of gut pacemaker activity and neuronal communication. We performed patch clamp on ICC-MY in situ to observe the changes of pacemaker activity in response to neural modulations. Methods: A fresh longitudinal muscle with myenteric plexus (LMMP) from mouse jejunum was prepared. ICC-MY and ganglion neurons embedded in the layer of longitudinal muscles were targeted by patch clamping in whole-cell configuration in a model of current or voltage clamp. Neurogenic modulators were applied to evaluate their effects on ICC pacemaker activity. Results: In situ ICC-MY showed spontaneous and rhythmical voltage oscillations with a frequency of 27.2 ± 3.9 cycles/min, amplitude of 32.6 ± 6.3 mV, and resting membrane potential of -62.2 ± 2.8 mV. In situ neurons showed electrically evocable action potential in single or multiple spikes. Pacemaker activity was modulated by neuronal activators through receiving a neuronal input. Application of tetrodotoxin depolarized pacemaker potentials in a dose dependent manner, and decreased the amplitude at tetrodotoxin 0.3 µM for about 40 ± 10%; capsaicin (1 µM) ameliorated ICC-MY K⁺ current for about 49 ± 14.8%; and, nitric oxide hyperpolarized pacemaker potential and decreased the amplitude and frequency. Conclusions: The in situ preparation patch clamp study further demonstrates that the pacemaker activity is an intrinsic property of ICC. The neurogenic activators change and shape pacemaker potential and activity in situ. LMMP preparation in situ patch clamp provides an ideal platform to study the functional innervation of the ICC and the enteric neural system, thereby, for evaluating the neural regulation of pacemaker activity, especially in disorder models.

4.
Oxid Med Cell Longev ; 2016: 7864150, 2016.
Artigo em Inglês | MEDLINE | ID: mdl-27847555

RESUMO

Acute pancreatitis (AP) is characterized by early activation of intra-acinar proteases followed by acinar cell death and inflammation. Cellular oxidative stress is a key mechanism underlying these pathological events. Sulforaphane (SFN) is a natural organosulfur antioxidant with undescribed effects on AP. Here we investigated modulatory effects of SFN on cellular oxidation and inflammation in AP. AP was induced by cerulean hyperstimulation in BALB/c mice. Treatment group received a single dose of 5 mg/kg SFN for 3 consecutive days before AP. We found that SFN administration attenuated pancreatic injury as evidenced by serum amylase, pancreatic edema, and myeloperoxidase, as well as by histological examination. SFN administration reverted AP-associated dysregulation of oxidative stress markers including pancreatic malondialdehyde and redox enzymes superoxide dismutase (SOD) and glutathione peroxidase (GPx). In acinar cells, SFN treatment upregulated nuclear factor erythroid 2-related factor 2 (Nrf2) expression and Nrf2-regulated redox genes including quinoneoxidoreductase-1, heme oxidase-1, SOD1, and GPx1. In addition, SFN selectively suppressed cerulein-induced activation of the nucleotide-binding domain leucine-rich repeat containing family, pyrin domain-containing 3 (NLRP3) inflammasome, in parallel with reduced nuclear factor- (NF-) κB activation and modulated NF-κB-responsive cytokine expression. Together, our data suggested that SFN modulates Nrf2-mediated oxidative stress and NLRP3/NF-κB inflammatory pathways in acinar cells, thereby protecting against AP.


Assuntos
Células Acinares/patologia , Inflamação/patologia , Isotiocianatos/farmacologia , Fator 2 Relacionado a NF-E2/metabolismo , Proteína 3 que Contém Domínio de Pirina da Família NLR/metabolismo , Estresse Oxidativo/efeitos dos fármacos , Pâncreas/patologia , Substâncias Protetoras/farmacologia , Células Acinares/efeitos dos fármacos , Células Acinares/metabolismo , Animais , Antioxidantes/metabolismo , Ceruletídeo , Citocinas/metabolismo , Citoproteção/efeitos dos fármacos , Inflamassomos/metabolismo , Mediadores da Inflamação/metabolismo , Isotiocianatos/administração & dosagem , Isotiocianatos/uso terapêutico , Camundongos Endogâmicos BALB C , NF-kappa B/metabolismo , Pancreatite/tratamento farmacológico , Pancreatite/patologia , Transdução de Sinais/efeitos dos fármacos
5.
Dalton Trans ; 44(33): 14763-70, 2015 Sep 07.
Artigo em Inglês | MEDLINE | ID: mdl-26219637

RESUMO

This article presents a combination strategy of electrodeposition and a layer-by-layer assembly to fabricate functional composite films with luminescence switching behavior. Firstly, a novel green luminescence film consisting of 8-hydroxypyrene-1,3,6-trisulfonic acid trisodium salt (HOPTS) was first obtained on ITO by a facile electrodeposition method. Then, the multilayer films containing different layers of tungstophosphate K12.5Na1.5[NaP5W30O110]·15H2O (P5W30) were further fabricated on the green luminescence film to form the composite films [(HOPTS)50/(PDDA/P5W30)n] (n = 10, film 1; n = 27, film 2; n = 57, film 3). Cyclic voltammetry and fluorescence spectroscopy were used to characterize the electrochemical activity of P5W30 and the luminescence property of HOPTS in the composite films, respectively. Lastly, in situ UV-Vis spectroelectrochemical and fluorescence spectroelectrochemical measurements were applied to investigate the luminescence switching behaviors of the composite films controlled by the electrochromism component of P5W30 upon electrochemical modulation. In summary, the investigation results revealed that the electrodeposition method is convenient and rapid, and thus-prepared composite films showed improved luminescence switching performance in terms of switching process, activation cycles, coloration efficiency, and bleached-state transparency as well as good stability, wide voltage range and good reversibility. Therefore, the present study offers a new fabrication route for the multifunctional composite films through an effective combination of electrodeposition and layer-by-layer assembly technique.

6.
J Surg Res ; 195(2): 529-40, 2015 May 15.
Artigo em Inglês | MEDLINE | ID: mdl-25752214

RESUMO

BACKGROUND: Vascular hyporeactivity plays an important role in severe trauma and shock. We investigated the beneficial effect of cyclosporine A (CsA) on traumatic shock and its relationship to vascular reactivity improvement and mitochondrial permeability transition pore (MPTP). MATERIALS AND METHODS: Sodium pentobarbital-anesthetized rats were used to induce traumatic hemorrhagic shock by left femur fracture and hemorrhage, the beneficial effects of CsA (1, 5, and 10 mg/kg, intravenously) on animal survival, cardiovascular function, tissue blood perfusion, and mitochondrial function of vital organs were observed. In addition, hypoxia-treated vascular smooth muscle cells from normal rats were used to investigate the relationship of this beneficial effect of CsA to Rho-associated serine/threonine kinase (ROCK) and protein kinase C. RESULTS: CsA prolonged the survival time and increased the 24-h survival rate of traumatic hemorrhagic shock (31%, 56%, and 56% in 1, 5, and 10 mg/kg CsA group versus 25% in lactated Ringer solution group). Five milligrams per kilogram of CsA had the best effect, which stabilized and improved the hemodynamics, increased the tissue blood flow, and improved the liver and kidney function including its mitochondrial function in shock rats. CsA had no significant influences on the production of inflammatory mediators and cardiac output after traumatic hemorrhagic shock. Further results indicated that CsA significantly improved the vascular constriction and dilation reactivity of superior mesenteric artery to norepinephrine and acetylcholine, which was antagonized by ROCK inhibitor, Y27632, but not by protein kinase C inhibitor, staurosporine. Further studies showed that CsA restored hypoxia-induced decrease of ROCK activity and inhibited the opening of MPTP in hypoxia-treated vascular smooth muscle cells. CONCLUSIONS: CsA is beneficial for the treatment of traumatic hemorrhagic shock. The mechanism is mainly through improving the vascular reactivity, stabilizing the hemodynamics, and increasing tissue perfusion. This beneficial effect of CsA is related to the inhibitory effect of CsA on MPTP opening. ROCK is an important regulator molecule in this process.


Assuntos
Ciclosporina/uso terapêutico , Choque Hemorrágico/tratamento farmacológico , Choque Traumático/tratamento farmacológico , Animais , Citocinas/sangue , Feminino , Hemodinâmica , Concentração de Íons de Hidrogênio , Rim/fisiopatologia , Ácido Láctico/sangue , Fígado/fisiopatologia , Masculino , Mitocôndrias/fisiologia , Proteína Quinase C/fisiologia , Ratos , Ratos Sprague-Dawley , Choque Hemorrágico/fisiopatologia , Choque Traumático/fisiopatologia , Quinases Associadas a rho/fisiologia
7.
Cell Mol Neurobiol ; 33(8): 1109-21, 2013 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-24002177

RESUMO

14-3-3 proteins have been confirmed to be involved in Parkinson's disease. It has been reported that an increase of 14-3-3 (theta, epsilon, and gamma) expression has neuroprotective effect in response to rotenone and MPP(+) in dopaminergic cell culture and transgenic C. elegans with alpha-synuclein overexpression. To further investigate the detail mechanism of 14-3-3 proteins in rotenone-induced dopamine neurotoxicity, we observed the expression of 14-3-3 isoforms, and the influence of 14-3-3epsilon knockdown on autophagic activity and cell function. The results showed that rotenone led to a decrease in expression of 14-3-3 protein and mRNA, and an increase in expression and aggregation of alpha-synuclein protein. Knockdown of 14-3-3epsilon expression in turn further aggravated PC12 cell damage, such as an enhancement of ROS formation, and a reduction of cell viability and ATP production. Further experiments confirmed that the autophagic activity was promoted with 14-3-3epsilon siRNA transfection, including an enhancement of autophagosome formation and the ratio of LC3-II/LC3-I. Therefore, we concluded that the regulation of 14-3-3 proteins in rotenone-induced neurotoxicity might be associated with its isoform 14-3-3epsilon's involvement in autophagy, which might be considered a mechanism in addition to the currently known function of 14-3-3 proteins in neurodegenerative disease pathogenesis.


Assuntos
Proteínas 14-3-3/metabolismo , Autofagia/efeitos dos fármacos , Neurotoxinas/toxicidade , Rotenona/toxicidade , Proteínas 14-3-3/genética , Trifosfato de Adenosina/metabolismo , Animais , Autofagia/genética , Forma Celular/efeitos dos fármacos , Forma Celular/genética , Sobrevivência Celular/efeitos dos fármacos , Sobrevivência Celular/genética , Regulação da Expressão Gênica/efeitos dos fármacos , Proteínas Associadas aos Microtúbulos/metabolismo , Células PC12 , Fagossomos/efeitos dos fármacos , Fagossomos/metabolismo , Isoformas de Proteínas/genética , Isoformas de Proteínas/metabolismo , Estrutura Quaternária de Proteína , RNA Mensageiro/genética , RNA Mensageiro/metabolismo , RNA Interferente Pequeno/metabolismo , Ratos , Espécies Reativas de Oxigênio/metabolismo , Transfecção , alfa-Sinucleína/metabolismo
8.
J Toxicol Pathol ; 26(2): 149-57, 2013 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-23914057

RESUMO

Rotenone is an inhibitor of mitochondrial complex I that produces a model of Parkinson's disease (PD), in which neurons undergo dopamine release dysfunction and other features. In neurons, exocytosis is one of the processes associated with dopamine release and is dependent on Ca(2+) dynamic changes of the cell. In the present study, we have investigated the exocytosis of dopamine and the involvement of Ca(2+) in dopamine release in PC12 cells administrated with rotenone. Results demonstrated that rotenone led to an elevation of intracellular Ca(2+) through Ca(2+) influx by opening of the voltage-gated Ca(2+) channel and influenced the soluble N-ethylmaleimide attachment protein receptor (SNARE) proteins expression (including syntaxin, vesicle-associated membrane protein 2 (VAMP2) and synaptosome-associated protein 25 (SNAP-25)); pretreatment with a blocker of L-type voltage-activated Ca(2+) channels (nifedipine) decreased the intracellular dopamine levels and ROS formation, increased the cell viability and enhanced the neurite outgrowth and exocytosis of synaptic vesicles. These results indicated that the involvement of intracellular Ca(2+) was one of the factors resulting in suppression of dopamine release suppression in PC12 cells intoxicated with rotenone, which was associated with the rotenone-induced dopamine neurotoxicity.

9.
Neurosci Biobehav Rev ; 36(9): 2034-43, 2012 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-22771336

RESUMO

Neurons are metabolically active cells with high energy demands. Thus, neurons are particularly reliant on mitochondrial function, especially on the homeostasis properties of mitochondria. This is reflected by the observation that mitochondrial abnormalities have been well recognized to contribute to neurodegenerative diseases, like Parkinson's disease (PD). Mitochondria are highly complex and dynamic organelles continuously undergoing different alterations. The dynamic property of mitochondria is named as mitochondrial homeostasis. Imbalance of mitochondrial homeostasis is associated with neurodegenerative disease, such as Parkinson's diseases. Recently, the related genes of PD-familial, such as alpha-synuclein, Parkin, PINK1, DJ-1 and LRRK2, are observed to be associated with mitochondria, and capable of modulating normal mitochondrial integrity and functions under certain conditions. Therefore, in this review, we will focus on the action of PD-related genes in mitochondrial homeostasis.


Assuntos
Homeostase/genética , Mitocôndrias/genética , Doença de Parkinson/genética , Humanos , Peptídeos e Proteínas de Sinalização Intracelular/genética , Peptídeos e Proteínas de Sinalização Intracelular/metabolismo , Serina-Treonina Proteína Quinase-2 com Repetições Ricas em Leucina , Mitocôndrias/metabolismo , Neurônios/metabolismo , Proteínas Oncogênicas/genética , Proteínas Oncogênicas/metabolismo , Doença de Parkinson/metabolismo , Proteína Desglicase DJ-1 , Proteínas Quinases/genética , Proteínas Quinases/metabolismo , Proteínas Serina-Treonina Quinases/genética , Proteínas Serina-Treonina Quinases/metabolismo , Ubiquitina-Proteína Ligases/genética , Ubiquitina-Proteína Ligases/metabolismo , alfa-Sinucleína/genética , alfa-Sinucleína/metabolismo
10.
Dalton Trans ; 39(23): 5439-45, 2010 Jun 21.
Artigo em Inglês | MEDLINE | ID: mdl-20431829

RESUMO

Two new homochiral inorganic-organic hybrid frameworks [Zn(HPO(3))(C(11)N(2)O(2)H(12))] (denoted as ZnHPO-CJ56) and [Zn(3)(H(2)O)(PO(4))(HPO(4))(C(6)H(9)N(3)O(2))(2)(C(6)H(8)N(3)O(2))] (denoted as ZnPO-CJ57) have been hydrothermally synthesized in the presence of chiral amino acids l-trypophan and l-histidine. Both of their inorganic networks are featured by one-dimensional (1D) edge-sharing Zn(2)P(2) ladder-like chains. The amino acid molecules as the ligands are grafted onto two sides of the chain. Extensive N-HO and O-HO hydrogen bonds of host-guest are formed to stable the chiral structures of ZnHPO-CJ56 and ZnPO-CJ57. It is noteworthy that the original chirality of the amino acid molecules is maintained in the structures of the as-synthesized compounds, and the resulting crystals have an enantiometric excess, which is confirmed by the solid state vibrational circular dichroism (VCD). Their syntheses, structures, and luminescence properties have been studied in detail. The formation of such chiral one-dimensional structures with multi-amino acids might be potentially applied in chiral catalysis, biochemistry processes or as functional materials.


Assuntos
Histidina/química , Fosfatos/química , Fosfitos/química , Triptofano/química , Compostos de Zinco/química , Dicroísmo Circular , Cristalografia por Raios X , Ligantes , Conformação Molecular
11.
Environ Toxicol Pharmacol ; 27(3): 366-72, 2009 May.
Artigo em Inglês | MEDLINE | ID: mdl-21783966

RESUMO

Rotenone, a mitochondrial complex-I inhibitor, has been verified to cause dopaminergic neurons degeneration in vivo and in vitro, and the substantia nigra pars compacta (SNc) and the striatum are the main target organs of rotenone in the rat brain. However, whether rotenone could cause damage to other regions in the brain has been unclear till now. To address this question, the rotenone-induced neurotoxicity in the hippocampal neurons was investigated in the present study. Rotenone (4mg/kg) was given to the male Sprague-Dawley rats per day for up to 4 weeks by using the osmotic minipumps. Results showed that neurodegeneration was formed and phosphorylated ERK1/2 (p-ERK1/2) was induced in the hippocampus of rats following rotenone treatment. In additionally, Ras, PKA and PKC were also activated and free [Ca(2+)](i) was increased in the cytoplasm of the hippocampus neurons. To determine how ERK cascade was activated, studies in the primary cultured hippocampus neurons were carried out in a further. Cell viability was reduced, and also apoptosis was induced in vitro following rotenone administration. Expressions of p-ERK1/2 were also enhanced evidently in the cultured neurons treated by rotenone. Free [Ca(2+)](i) was also increased in the cultured neurons induced by rotenone. However, this influx might not take main effect in ERK1/2 phosphorylation. In conclusion, Ras-Raf-1-MEK-ERK1/2 classic signal pathway, not by PKA/PKC alternative pathway may be the mainly contributor to the ERK1/2 phosphorylation. And also, Ras protein is the dominant activator in the ERK phosphorylation induced by rotenone.

12.
Toxicol In Vitro ; 22(6): 1461-8, 2008 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-18579341

RESUMO

Rotenone is a widely used pesticide. Administration of rotenone can induce biochemical and histological alterations similar to those of Parkinson's disease in rats, leading to the selective loss of dopaminergic neurons in the substantia nigra pars compacta. However, it remains unclear why rotenone seems to affect preferentially dopaminergic cells. To address this question, we studied the effects of rotenone on dopamine distribution and metabolism to determine the role of endogenous dopamine in rotenone-induced PC12 cells toxicity. Results showed that cell viability was decreased and intracellular dopamine concentration was increased with rotenone administration in a dose-dependent manner. Rotenone exposure led to changes of proteins and enzymes associated with dopamine synthesis and transportation in PC12 cells. Tyrosine hydroxylase (TH) and vesicular monoamine transporter 2 (VMAT(2)) were markedly down-regulated, and dopamine transporter (DAT) was up-regulated in the cells. The activity of monoamine oxidase (MAO) was also increased. In addition, rotenone increased ROS formation, which was clearly inhibited by the pretreatment of GSH. Similar inhibitions of ROS formation were also observed in PC12 cells pretreated with the classical dopamine transporter inhibitor of GBR-12909 and the MAO inhibitor L-deprenyl. Moreover, opposite effects were observed in PC12 cells pretreated with the specific VMAT(2) inhibitor reserpine. These results suggest that rotenone administration may interfere with dopamine distribution and metabolism, leading to dopamine accumulated in the cytoplasm of PC12 cells, which may contribute to the ROS formation and cell death. Therefore, the endogenous dopamine resulted from the altered dopamine metabolism and redistribution may play an important role in rotenone toxicity in dopamine neurons.


Assuntos
Dopamina/metabolismo , Inseticidas/toxicidade , Estresse Oxidativo/efeitos dos fármacos , Rotenona/toxicidade , Animais , Transporte Biológico , Morte Celular/efeitos dos fármacos , Sobrevivência Celular/efeitos dos fármacos , Citoplasma/metabolismo , Relação Dose-Resposta a Droga , Regulação da Expressão Gênica/efeitos dos fármacos , Inseticidas/administração & dosagem , Neurônios/efeitos dos fármacos , Neurônios/metabolismo , Células PC12 , Ratos , Espécies Reativas de Oxigênio/metabolismo , Rotenona/administração & dosagem
13.
Zhongguo Wei Zhong Bing Ji Jiu Yi Xue ; 18(12): 755-8, 2006 Dec.
Artigo em Chinês | MEDLINE | ID: mdl-17166360

RESUMO

OBJECTIVE: To plan and develop a Chongqing chemical accident rescue command system. METHODS: Based on the modes of leakage and diffusion of various poisonous gases and chemicals, different modes of injuries produced, and their appropriate rescue and treatments, also taking the following factors such as the condition of storage of chemicals, meteorological and geographic conditions, medical institutions and equipment, and their rescuing capacity into consideration, a plan was drafted to establish the rescue system. Real-time simulation technology, data analysis, evaluation technology and database technology were employed in the planning. Using Visual Studio 6.0 as the software development platform, this project aimed to design the software of an emergency command system for chemical accidents in Chongqing which could be operated with the Windows 2000/XP operating system. RESULTS: This system provided a dynamic scope of the endangered area, casualty number estimates, and recommendation of measures and a rescue plan for various chemical accidents. Furthermore, the system helped retrieve comprehensive information regarding the physical and chemical characteristics of more than 4 200 dangerous poisonous chemicals and their appropriate treatment modalities. CONCLUSION: This system is easy to operate with a friendly interface, functions rapidly and can provide real-time analysis with comparatively precise results. This system could satisfy the requirements of executing the command and the rescue of a chemical accident with good prospects of application.


Assuntos
Acidentes , Sistemas de Apoio a Decisões Administrativas , Serviços Médicos de Emergência/organização & administração , Substâncias Perigosas , Software , China , Humanos , Interface Usuário-Computador
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