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1.
Nanotechnology ; 28(46): 465602, 2017 11 17.
Artigo em Inglês | MEDLINE | ID: mdl-29053476

RESUMO

In this work, a solution combustion followed by dissolution in hydrogen peroxide is adopted to achieve a precursor for decorating anatase TiO2 nanosheets along single-crystalline rutile TiO2 nanorods, which achieves balsam-pear-like core/shell nanorod arrays with enhanced photoelectrochemical water splitting. The enhanced photoelectrochemical performance is attributed to the novel nanoarchitecture, which can simultaneously offer a high surface area, enhanced light-harvesting, a rutile/anatase junction for charge carrier separation and a conductive pathway for charge carrier collection. The photoanode design can also give hints to other functional materials.

2.
Basic Clin Pharmacol Toxicol ; 104(6): 434-40, 2009 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-19489787

RESUMO

Rho kinase inhibition is beneficial for neurite outgrowth and nerve disorders, and the Rho kinase inhibitors have been regarded as promising agents to treat neural diseases. The main aim of the study was to elucidate how Rho kinase inhibitor Y-27632 regulates neurotransmitter norepinephrine synthesis and release in PC12 cells when neurite outgrowth was induced. PC12 cells were treated with Y-27632 for 6 days. The amount of norepinephrine synthesized in PC12 cells and the amount released evoked by acetylcholine or by KCl were determined by norepinephrine enzyme-linked immunosorbent assay kits. The results showed that the amount of norepinephrine both synthesized and released was down-regulated with a concentration-dependent relationship. Further results of Western blotting found that the protein expression of tyrosine hydroxylase and synapsin I (especially its active form, synapsin I phosphoSer603) was also down-regulated, which were directly related to synthesis and release of norepinephrine, respectively. All the results suggest that Y-27632 is able to down-regulate norepinephrine synthesis and release, the direct mechanism of which may be associated with down-regulation on expression of some proteins, including tyrosine hydroxylase and synapsin I.


Assuntos
Amidas/farmacologia , Neuritos/efeitos dos fármacos , Norepinefrina/antagonistas & inibidores , Piridinas/farmacologia , Quinases Associadas a rho/antagonistas & inibidores , Acetilcolina/farmacologia , Animais , Western Blotting , Relação Dose-Resposta a Droga , Regulação para Baixo , Ensaio de Imunoadsorção Enzimática , Fator de Crescimento Neural/farmacologia , Neuritos/metabolismo , Norepinefrina/biossíntese , Células PC12 , Cloreto de Potássio/farmacologia , Ratos
3.
J Pharm Pharmacol ; 60(2): 205-11, 2008 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-18237468

RESUMO

We have investigated the antiproliferative effects of TBIDOM (N-(4-(2,2,2-trifluoroethyl) benzylidene) (7-isopropyl-1,4a-dimethyl-1,2,3,4,4a,9,10,10a-octahydrophenanthren-1-yl) meth-anamine) and have explored its possible mechanisms on human hepatocellular carcinoma SMMC-7721 cells. The proliferative status of cells treated with TBIDOM was measured by the colorimetric MTT assay. Cellular apoptosis was analysed using Hoechst 33342 staining and flow cytometry. Reduction of mitochondrial membrane potential (Delta psi(m)) was also detected by flow cytometry. Western blotting assay was used to evaluate the release of cytochrome c and expression of p53, Bcl-2 and Bax proteins. It was shown that TBIDOM displayed a significant inhibitory effect on growth of SMMC-7721 cells in a dose- and time-dependent manner. Hoechst 33342 staining and flow cytometry analysis showed an increase of apoptosis rate and decrease of mitochondrial membrane potential after SMMC-7721 cells were exposed to TBIDOM for 24 h. Pretreatment of SMMC-7721 cells with TBIDOM significantly induced a decrease of Bcl-2 protein expression and an increase of caspase-3 activity and Bax protein expression. The results indicated that TBIDOM could effectively inhibit proliferation by induction of apoptosis and could be a promising candidate in the development of a novel class of antitumour agent.


Assuntos
Abietanos/farmacologia , Antineoplásicos/farmacologia , Compostos de Benzil/farmacologia , Carcinoma Hepatocelular/tratamento farmacológico , Neoplasias Hepáticas/tratamento farmacológico , Abietanos/administração & dosagem , Antineoplásicos/administração & dosagem , Apoptose , Compostos de Benzil/administração & dosagem , Western Blotting , Caspase 3/efeitos dos fármacos , Caspase 3/metabolismo , Linhagem Celular Tumoral , Proliferação de Células/efeitos dos fármacos , Colorimetria , Relação Dose-Resposta a Droga , Citometria de Fluxo , Regulação da Expressão Gênica/efeitos dos fármacos , Humanos , Potencial da Membrana Mitocondrial/efeitos dos fármacos , Proteínas Proto-Oncogênicas c-bcl-2/efeitos dos fármacos , Proteínas Proto-Oncogênicas c-bcl-2/metabolismo , Fatores de Tempo , Proteína X Associada a bcl-2/efeitos dos fármacos , Proteína X Associada a bcl-2/metabolismo
4.
Yakugaku Zasshi ; 127(3): 527-32, 2007 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-17329938

RESUMO

Cyclooxygenase 2 (COX-2) pathway inhibitors were regarded as promising nonsteroidal antiinflammatory drugs (NSAIDs). We discovered that the COX-2 pathway in A549 cells, a human lung cancer cell line, was activated by serum-free stimulation, and a drug screening model for NSAIDs was established based on this principle with simple performance and sufficient reliability. The COX-2 pathway was activated by treating with serum-free medium for 12 h. The activated cells were incubated with NS398 (selective COX-2 inhibitor), SC560 (selective COX-1 inhibitor), acetyl salicylic acid (ASA) (nonselective COX inhibitor) at 37 degrees C for 15 min. Then the cells were incubated with 10 microM of arachidonic acid (AA) for another 30 min prostaglandin E2 and 6-keto-prostaglandin F(1alpha) were assayed in an enzyme immunoassay (EIA). The results showed that the COX-2 pathway was dominant in A549 cells whether activated by serum-free medium or not, and the COX-1 pathway could be ignored. The model accepted the positive inhibition threshold as NS398 2 microM; if a compound (10 microM) inhibited COX-2 pathway more than NS398 (2 microM), it was regarded as a hit. The COX-2 pathway inhibition experiment showed that the Z;-factor of the screening model was 0.62, which suggests that the model is suitable for COX-2 pathway inhibitor screening.


Assuntos
Anti-Inflamatórios não Esteroides/farmacologia , Inibidores de Ciclo-Oxigenase 2/farmacologia , Avaliação Pré-Clínica de Medicamentos/métodos , Nitrobenzenos/farmacologia , Pirazóis/farmacologia , Sulfonamidas/farmacologia , 6-Cetoprostaglandina F1 alfa/análise , Animais , Aspirina/farmacologia , Meios de Cultura Livres de Soro , Dinoprostona/análise , Relação Dose-Resposta a Droga , Humanos , Técnicas Imunoenzimáticas , Células Tumorais Cultivadas
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