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1.
J Asthma ; : 1-8, 2019 Oct 14.
Artigo em Inglês | MEDLINE | ID: mdl-31514546

RESUMO

Purpose: The aim of this study was to investigate the efficacy and safety of tratinterol hydrochloride in bronchial asthma (BA) treatment. Methods: Patients enrolled in this study were distributed randomly into a treatment group (tratinterol hydrochloride) and an active control group (procaterol hydrochloride) and were treated for 2 weeks after running-in. The end points were changes in pulmonary function and clinical symptoms after administration. Safety indices were physical examinations, laboratory testing and spontaneous reporting. Findings: We enrolled 732 subjects, -365 in the treatment group and 367 in the active control group. Forced expiratory volume (FEV1), significantly increased in both group after treatment (P < 0.05). Least-squares (LS) means were -0.03/in the full-analysis set (FAS) and -0.02 in the per-protocol set (PPS) set, and 95% confidence intervals (CIs) for these sets were -0.09 to 0.03 and -0.08 to 0.04, respectively. Forced expiratory volume (FVC), morning peak expiratory flow (PEF) and asthma scores were significantly different with pretreatment (P < 0.05). There was no difference in asymptomatic days or frequency of relief medicine use (P > 0.05). No serious adverse events occurred. Implications: Tratinterol hydrochloride was effective, safe and not inferior to procaterol hydrochloride in treating BA.

2.
Fitoterapia ; 130: 48-53, 2018 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-30114468

RESUMO

Four novel and potently bioactive Amaryllidaceae alkaloids, 4,8-dimethoxy-cripowellin C (1), 4,8-dimethoxy-cripowellin D (2), 9-methoxy-cripowellin B (3), and 4-methoxy-8-hydroxy-cripowellin B (4), together with one known alkaloid, cripowellin C (5) were isolated from the 95% EtOH extract of the bulbs of Crinum latifolium. Structural elucidation of all the compounds were performed by spectral methods such as 1D and 2D (1H-1H COSY, HMQC, and HMBC) NMR as well as spectroscopy high resolution mass spectrometry. All isolates were in vitro evaluated for their cytotoxic activity against seven lung cancer cell lines, in addition to antimicrobial activity for eight bacteria, scavenging potential using ABTS·+ and DPPH test, and anti-inflammatory activity for Cox-1 and Cox-2 which had not previously been tested for crinane-type alkaloids with the cleavage between C-1 and C-13. Consequently, alkaloids 1-5 exhibited potent cytotoxicity against all of seven tested tumor cell lines with (IC50 < 30 nM). Alkaloids 3 and 4 displayed the significant antimicrobial activity with IC50 values <0.50 mM and antioxidant activity in the ABTS·+ and DPPH test. Additionally, Alkaloids 1-5 exhibited comparable inhibition of Cox-1 (>64%) and Cox-2 (>90%) with positive control.


Assuntos
Alcaloides/isolamento & purificação , Alcaloides/farmacologia , Crinum/química , Anti-Infecciosos/isolamento & purificação , Anti-Infecciosos/farmacologia , Anti-Inflamatórios/isolamento & purificação , Anti-Inflamatórios/farmacologia , Antineoplásicos Fitogênicos/isolamento & purificação , Antineoplásicos Fitogênicos/farmacologia , Antioxidantes/isolamento & purificação , Antioxidantes/farmacologia , Linhagem Celular Tumoral , China , Humanos , Estrutura Molecular , Compostos Fitoquímicos/isolamento & purificação , Compostos Fitoquímicos/farmacologia , Raízes de Plantas/química
3.
Environ Sci Pollut Res Int ; 25(19): 18392, 2018 07.
Artigo em Inglês | MEDLINE | ID: mdl-29869740

RESUMO

In the original article the authors list and the credit to the corresponding authors were not complete.

4.
Environ Sci Pollut Res Int ; 25(19): 18385-18391, 2018 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-29372517

RESUMO

MicroRNAs (miRNAs) have been shown to be critical regulators in many types of tumors. The aim of our study was to investigate the role of miR-760 in non-small cell lung cancer (NSCLC). We demonstrated that the expression of miR-760 was downregulated in NSCLC tissues compared with the adjacent normal tissues. We also demonstrated that the expression of miR-760 was downregulated in the NSCLC cell lines. Overexpression of miR-760 suppressed the NSCLC cell proliferation, cell cycle, and migration. Moreover, we identified that ROS1 was a direct target of miR-760 in the NSCLC cell. Elevated expression of miR-760 suppressed ROS1 expression in the NSCLC cell. We also demonstrated that the expression of ROS1 was higher in the NSCLC tissues than in the adjacent lung tissues. MiR-760 expression level was reversely associated with the expression level of ROS1 in the NSCLC tissues. In summary, we showed that miR-760 suppressed the NSCLC cell proliferation, cell cycle, and migration through regulating the ROS1 expression. These data suggested that miR-760 may act as a tumor suppressor gene in the NSCLC partly through regulating ROS1 expression.


Assuntos
Carcinoma Pulmonar de Células não Pequenas/genética , Proliferação de Células , Neoplasias Pulmonares/genética , MicroRNAs/genética , Proteínas Tirosina Quinases/metabolismo , Proteínas Proto-Oncogênicas/metabolismo , Carcinoma Pulmonar de Células não Pequenas/metabolismo , Carcinoma Pulmonar de Células não Pequenas/patologia , Linhagem Celular Tumoral , Regulação para Baixo , Regulação Neoplásica da Expressão Gênica , Humanos , Neoplasias Pulmonares/metabolismo , Neoplasias Pulmonares/patologia , Proteínas Tirosina Quinases/genética , Proteínas Proto-Oncogênicas/genética , Regulação para Cima
5.
Am J Transl Res ; 10(12): 4193-4201, 2018.
Artigo em Inglês | MEDLINE | ID: mdl-30662662

RESUMO

LncRNAs play significant roles in various cell biological processes. In the present study, we demonstrated that PICART1 expression was down-regulated in non-small cell lung cancer (NSCLC) tissues. Lower expression level of PICART1 was associated with advanced stage. In addition, PICART1 expression was down-regulated in NSCLC cell lines. Overexpression of PICART1 inhibited NSCLC cell growth and induced cell cycle arrest at G2/M phase. Elevated expression of PICART1 suppressed NSCLC cell colony formation and cell invasion. Ectopic expression of PICART1 promoted the expression of epithelial marker E-cadherin while suppressed the mesenchymal marker expression such as N-cadherin and Snail and Vimentin. Furthermore, PICART1 overexpression suppressed AKT phosphorylation and c-Myc expression while inhibited the p21 expression in NSCLC cell. AKT phosphorylation was involved in PICART1 mediated suppression of cell growth and invasion. These results suggested that overexpression of PICART1 suppressed cell growth and invasion partly through regulating AKT signaling pathway in NSCLC.

6.
Clin Ther ; 37(6): 1248-58, 2015 Jun 01.
Artigo em Inglês | MEDLINE | ID: mdl-25857594

RESUMO

PURPOSE: The aim of this study was to determine the efficacy and safety profile of tratinterol hydrochloride tablets in the treatment of bronchial asthma. METHODS: This multicenter, randomized, double-blind clinical research study was completed at 6 centers in the People's Republic of China from March 2009 to June 2010, and a randomized trial of procaterol hydrochloride tablets produced by Otsuka Pharmaceutical Co Ltd was conducted. The study was approved by the Medical Ethics Committee of the First Hospital of China Medical University. The clinical trial registration number is 2007L04263. FINDINGS: A total of 223 patients were selected for this study, with 112 patients in the treatment group and 111 in the control group. The lung function of the 2 groups after treatment significantly increased in all (P < 0.05); however, there was no significant difference in the changes between the 2 groups (P > 0.05). The occurrence of related adverse events at varying degrees in the control group was higher than in the treatment group. IMPLICATIONS: It is safe and effective to use tratinterol hydrochloride tablets to treat bronchial asthma.


Assuntos
Compostos de Anilina/uso terapêutico , Asma/tratamento farmacológico , Broncodilatadores/uso terapêutico , Álcool Feniletílico/análogos & derivados , Adulto , Compostos de Anilina/efeitos adversos , Asma/fisiopatologia , Broncodilatadores/efeitos adversos , China , Método Duplo-Cego , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Álcool Feniletílico/efeitos adversos , Álcool Feniletílico/uso terapêutico , Procaterol/uso terapêutico , Testes de Função Respiratória , Comprimidos
7.
Int J Clin Exp Pathol ; 8(1): 361-7, 2015.
Artigo em Inglês | MEDLINE | ID: mdl-25755723

RESUMO

BACKGROUND AND AIM: Lung cancer is one of leading malignant tumor worldwide with a high mortality rate. A new therapy target, enhancer of polycomb1 (EPC1) knocked down by short hairpin RNA (shRNA) interference technology, for lung cancer was established to investigate its effects on lung cancer in present study. METHODS: RNA interference technology was applied to down-regulate the expression of EPC1 by specific-shRNA with lentivirus vector in neoplastic human alveolar basal epithelial cells (A549 cells). The survival rate and apoptosis were respectively measured by MTT and Flow Cytometry to evaluate the effects of shRNA EPC1 on cells. Mice xenografts of HCT116 cells with shRNA EPC1 were also established to assess the effect on tumor growth. The levels of AKT and p65 were detected by western blotting. RESULTS: The down-regulation of EPC1 by specific-shRNA with lentivirus vector was significantly decreased the survival rate and apoptosis of A549 cells, and the tumors in EPC1 shRNA transfection group had a significant lower size and weight compared with the ones with control shRNA. The protein expression of p-AKT and p65 was reduced by EPC1 shRNA in both in vitro and in vivo experiments. CONCLUSION: Silencing EPC1 by shRNA technology had the inhibition effects on cell proliferation and tumor growth in lung cancer, which provided a new potential target for treatment of cancers.


Assuntos
Apoptose/genética , Proteínas Cromossômicas não Histona/biossíntese , Neoplasias Pulmonares/patologia , RNA Interferente Pequeno , Proteínas Repressoras/biossíntese , Animais , Western Blotting , Linhagem Celular Tumoral , Citometria de Fluxo , Técnicas de Silenciamento de Genes , Humanos , Camundongos , Camundongos Endogâmicos BALB C , Interferência de RNA , Reação em Cadeia da Polimerase em Tempo Real , Transfecção , Ensaios Antitumorais Modelo de Xenoenxerto
8.
Can J Physiol Pharmacol ; 90(12): 1576-84, 2012 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-23210436

RESUMO

We investigated the effects of arsenic trioxide (As(2)O(3)) as a possible approach for preventing airway remodeling in a murine model of bronchial asthma induced by ovalbumin (OVA) challenge. Forty Balb/c mice were randomly assigned to 1 of 4 groups (10 mice/group) as follows: controls (challenged with sterile saline inhalation only); OVA-challenged, no treatment; OVA-challenged, treated with dexamethasone; and OVA-challenged, treated with As(2)O(3). All mice were sensitized by intraperitoneal injection with 10% OVA at 2 weeks prior to saline or OVA inhalation challenge. Challenges were for 8 weeks. After OVA challenge, typical asthma-like morphology changes in the bronchi and lung tissues were observed by hematoxylin-eosin staining and pulmonary function indices were reduced compared with controls. Changes in pulmonary indices and lung tissues were similar in the dexamethasone and As(2)O(3) groups and were in between those of the untreated and control groups. Compared with the untreated group, transforming growth factor ß1, vascular endothelial growth factor, and matrix metalloproteinase-9 protein levels and mRNA expression were decreased in lung tissues of the dexamethasone and As(2)O(3) groups. Our results suggest that steroids and As(2)O(3) can inhibit airway remodeling in chronic asthma by mechanisms related to inhibiting the expression of the 3 aforementioned mediators.


Assuntos
Remodelação das Vias Aéreas/efeitos dos fármacos , Arsenicais/farmacologia , Asma/tratamento farmacológico , Brônquios/efeitos dos fármacos , Pulmão/efeitos dos fármacos , Óxidos/farmacologia , Remodelação das Vias Aéreas/genética , Animais , Trióxido de Arsênio , Asma/genética , Asma/metabolismo , Asma/patologia , Brônquios/metabolismo , Brônquios/patologia , Dexametasona/farmacologia , Feminino , Pulmão/metabolismo , Pulmão/patologia , Metaloproteinase 9 da Matriz/genética , Metaloproteinase 9 da Matriz/metabolismo , Camundongos , Camundongos Endogâmicos BALB C , Ovalbumina/farmacologia , Distribuição Aleatória , Testes de Função Respiratória/métodos , Fator de Crescimento Transformador beta1/genética , Fator de Crescimento Transformador beta1/metabolismo , Fator A de Crescimento do Endotélio Vascular/genética , Fator A de Crescimento do Endotélio Vascular/metabolismo
9.
Zhonghua Jie He He Hu Xi Za Zhi ; 30(8): 573-6, 2007 Aug.
Artigo em Chinês | MEDLINE | ID: mdl-17988548

RESUMO

OBJECTIVE: To investigate the expressions of and the effect of smoking on vascular endothelial growth factor (VEGF) and induced nitric oxide synthase (iNOS) in lung tissues of chronic obstructive pulmonary disease (COPD) patients. METHODS: The peripheral lung tissues were obtained from 46 patients with lung carcinoma. They were divided into three groups according to their habit of smoking and lung function, 19 smokers with moderate COPD, 12 smokers and 15 nonsmokers with normal lung function. The expression of VEGF and iNOS was detected by immunohistochemistry. RESULTS: Expressions of VEGF and iNOS were increased in lung tissues of smokers without COPD (1.50 +/- 0.39, 1.45 +/- 0.41) compared with nonsmokers without COPD (1.18 +/- 0.33, 1.09 +/- 0.41) (each P < 0.05), and were significantly increased in lung tissues of smokers with moderate COPD (2.19 +/- 0.51, 2.39 +/- 0.45) compared with nonsmokers without COPD (each P < 0.01). The expression of VEGF in lung tissues was significantly correlated with the expression of iNOS (r = 0.78, P < 0.01), but was inversely correlated with FEV(1) (r = -0.67, P < 0.01). CONCLUSIONS: Expressions of VEGF and iNOS were upregulated in lung tissues of smokers and patients with moderate COPD. Overexpression of iNOS and VEGF may participate in the mechanism of airway and vascular remodeling, and airflow limitation in COPD.


Assuntos
Pulmão/metabolismo , Óxido Nítrico Sintase/metabolismo , Doença Pulmonar Obstrutiva Crônica/metabolismo , Fumar , Fator A de Crescimento do Endotélio Vascular/metabolismo , Adulto , Idoso , Feminino , Volume Expiratório Forçado , Humanos , Imuno-Histoquímica , Pulmão/patologia , Pulmão/fisiopatologia , Masculino , Pessoa de Meia-Idade , Miócitos de Músculo Liso/metabolismo , Miócitos de Músculo Liso/patologia , Doença Pulmonar Obstrutiva Crônica/patologia , Doença Pulmonar Obstrutiva Crônica/fisiopatologia , Capacidade Vital
10.
BMC Genomics ; 8: 332, 2007 Sep 22.
Artigo em Inglês | MEDLINE | ID: mdl-17888167

RESUMO

BACKGROUND: It becomes increasingly clear that our current taxonomy of clinical phenotypes is mixed with molecular heterogeneity. Of vital importance for refined clinical practice and improved intervention strategies is to define the hidden molecular distinct diseases using modern large-scale genomic approaches. Microarray omics technology has provided a powerful way to dissect hidden genetic heterogeneity of complex diseases. The aim of this study was thus to develop a bioinformatics approach to seek the transcriptional features leading to the hidden subtyping of a complex clinical phenotype. The basic strategy of the proposed method was to iteratively partition in two ways sample and feature space with super-paramagnetic clustering technique and to seek for hard and robust gene clusters that lead to a natural partition of disease samples and that have the highest functionally conceptual consensus evaluated with Gene Ontology. RESULTS: We applied the proposed method to two publicly available microarray datasets of diffuse large B-cell lymphoma (DLBCL), a notoriously heterogeneous phenotype. A feature subset of 30 genes (38 probes) derived from analysis of the first dataset consisting of 4026 genes and 42 DLBCL samples identified three categories of patients with very different five-year overall survival rates (70.59%, 44.44% and 14.29% respectively; p = 0.0017). Analysis of the second dataset consisting of 7129 genes and 58 DLBCL samples revealed a feature subset of 13 genes (16 probes) that not only replicated the findings of the important DLBCL genes (e.g. JAW1 and BCL7A), but also identified three clinically similar subtypes (with 5-year overall survival rates of 63.13%, 34.92% and 15.38% respectively; p = 0.0009) to those identified in the first dataset. Finally, we built a multivariate Cox proportional-hazards prediction model for each feature subset and defined JAW1 as one of the most significant predictor (p = 0.005 and 0.014; hazard ratios = 0.02 and 0.03, respectively for two datasets) for both DLBCL cohorts under study. CONCLUSION: Our results showed that the proposed algorithm is a promising computational strategy for peeling off the hidden genetic heterogeneity based on transcriptionally profiling disease samples, which may lead to an improved diagnosis and treatment of cancers.


Assuntos
Heterogeneidade Genética , Linfoma Difuso de Grandes Células B/genética , Análise por Conglomerados , Perfilação da Expressão Gênica , Humanos , Análise de Sequência com Séries de Oligonucleotídeos
11.
Zhongguo Fei Ai Za Zhi ; 7(3): 218-21, 2004 Jun 20.
Artigo em Chinês | MEDLINE | ID: mdl-21232222

RESUMO

BACKGROUND: To study the levels of expression, coexpression, and clinical significancer of four multidrug resistance factors in lung cancer. METHODS: The P glycoprotein (P-gp), multidrug-resistance-associated protein (MRP), lung resistance protein (LRP), glutathione S-transferase (GST-π) of 60 lung cancer patients were detected by using immunohistochemical method. RESULTS: The positive rate of the drug resistance factor was 53.3% (32/60), 63.3% (38/60), 70.0% (42/60), and 80.0% (48/60) for P-gp, MRP, LRP, and GST-π respectively. Patients with NSCLC had significantly higher expression of the drug resistance factors than those with SCLC. On the other hand, no relationship was observed between the expression of drug resistance factors and TNM stage and cell differentiation. The coexpression rate was as follows: P-gp+MRP, 41.6% ; P-gp+LRP, 35.0%; MRP+LRP, 53.3%; MRP+GST-π, 50.0%; LRP+GST-π, 58.3%; P-gp+GST-π, 45.0%; P-gp+MRP+LRP+GST-π, 20.0%. Among them, a relationship was detected between P-gp and MRP ( rs =0.756, P < 0.01), between P-gp and LRP ( rs =0.686, P < 0.01), between MRP and LRP ( rs =0.669, P < 0.01), between MRP and GST-π( rs =0.546, P < 0.01), between LRP and GST-π ( rs =0.848, P < 0.01), between P-gp and LRP ( rs =0.689, P < 0.01), and between P-gp and GST-π ( rs = 0.535 , P < 0.01). CONCLUSIONS: The MDR in lung cancer patients is affected by various multidrug resistance factors. The drug resistance factors' expression is related to histology, but not to TNM stage and cell differentiation.

12.
Zhonghua Jie He He Hu Xi Za Zhi ; 25(11): 665-6, 2002 Nov.
Artigo em Chinês | MEDLINE | ID: mdl-12490120

RESUMO

OBJECTIVE: To study the arsenic trioxide (As(2)O(3)) induced apoptosis in a human small cell lung cancer cell line (NeI-H cells) and its possible mechanisms. METHODS: Apoptotic cells were detected by the TUNEL method. The expression of p53 and bcl-2 was analyzed with immunohistochemical staining. RESULTS: NeI-H cells showed the sub-G(1) peak after treatment with As(2)O(3) (0.5 micromol/L, 1.0 micromol/L, and 2.0 micromol/L) for 72 hours. The ratio of apoptotic cells increased with the increasing concentrations of the drug and the time of culture. Immunohistochemical staining of NeI-H cells showed increased expression of p53, but decreased expression of bcl-2 with the increasing concentrations of the drug. CONCLUSION: The anti-carcinogenic effect of As(2)O(3) is due to the induction of cell apoptosis. Up-regulation of the p53 gene and down-regulation of the bcl-2 gene may be an underlining mechanism.


Assuntos
Antineoplásicos/farmacologia , Apoptose/efeitos dos fármacos , Arsenicais/farmacologia , Carcinoma de Células Pequenas/tratamento farmacológico , Genes bcl-2 , Genes p53 , Neoplasias Pulmonares/tratamento farmacológico , Óxidos/farmacologia , Trióxido de Arsênio , Carcinoma de Células Pequenas/genética , Carcinoma de Células Pequenas/patologia , Expressão Gênica/efeitos dos fármacos , Humanos , Neoplasias Pulmonares/genética , Neoplasias Pulmonares/patologia , Células Tumorais Cultivadas
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