Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 4 de 4
Filtrar
Mais filtros










Base de dados
Intervalo de ano de publicação
1.
Cancer Med ; 6(10): 2222-2233, 2017 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-28940986

RESUMO

Lentinan is a common biological response modifier. This study was sought to evaluate the efficacy of adjuvant lentinan combined with chemotherapy for advanced cancer. A meta-analysis of published prospective controlled trials investigating the effects of lentinan for kinds of advanced cancer was performed. Sensitivity analysis, inverted funnel plots, and trial sequence analysis were conducted to explore the reliability and stability of results. Seventeen clinical studies were identified containing 1423 patients. Twelve trials included gastrointestinal cancer (GIC), three trials included lung cancer (LC), and two trials included the two cancers. There was a increase in survival rate in 1 year (risk ratios [RR], 1.46, P = 0.001) and overall response rate including both complete and partial response (RR, 1.28, P = 0.005). There was also a reduction in progressive disease (RR, 0.57, P = 0.0005), nonsevere adverse events (RR, 0.88, P = 0.004), and severe adverse events (RR, 0.73, P = 0.007). Similar results were shown in the two subgroups of GIC and LC. Limited trials reported the data of median overall survival and time to treatment failure, and the data were insufficient for quantitative analysis, and no significant difference were found in 2-year survival rate. Adjuvant lentinan used with chemotherapy achieved improvements in 1-year survival rate, response rate, and adverse events in advanced cancer. The effect seemed to be similar irrespective of cancer type. However, its sustained efficacy on survival was still unclear.


Assuntos
Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico , Neoplasias/tratamento farmacológico , Neoplasias/patologia , Antineoplásicos/administração & dosagem , Protocolos de Quimioterapia Combinada Antineoplásica/efeitos adversos , Progressão da Doença , Humanos , Fatores Imunológicos/administração & dosagem , Lentinano/administração & dosagem , Estadiamento de Neoplasias , Neoplasias/mortalidade , Viés de Publicação , Análise de Sobrevida , Falha de Tratamento , Resultado do Tratamento
2.
Int J Mol Med ; 30(6): 1443-50, 2012 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-23042547

RESUMO

The activation of hepatic stellate cells (HSCs) is closely associated with liver fibrosis in chronic hepatitis B virus (HBV) infection. However, the molecular mechanisms leading to HSC activation remain unclear. It has been reported that the platelet-derived growth factor-B (PDGF-B)/PDGF receptor-ß (PDGFR-ß) signaling pathway is involved in this process. Thus, we investigated whether HBV and its protein contribute to HSC proliferation by the PDGF-B/PDGFR-ß signaling pathway. HBV particles were purified from the supernatant of HepG2.2.15 cells by ultracentrifugation and the cell lines carrying HBV preS, e, c or x genes were obtained. After incubation with HBV particles or co-cultured with the cell lines expressed in the viral protein, the proliferation of LX-2 cells, an HSC cell line, were detected by flow cyto-metry and real-time PCR and the expression of molecules related to the PDGF-B/PDGFR-ß signaling pathway were further measured. Our results indicated that HBV particles, c and x proteins promoted LX-2 proliferation and increased the mRNA levels of PDGF-B, PDGFR-ß, collagen-I and α-smooth muscle actin (α-SMA), as well as the phosphorylation of PDGFR-ß; however, the expression protein levels of PDGF-B and PDGFR-ß remained unchanged. In conclusion, HBV particles and HBV c and x proteins promote HSC proliferation and fibrogenesis in vitro and the PDGF-B/PDGFR-ß signaling pathway is important in this process.


Assuntos
Células Estreladas do Fígado/fisiologia , Vírus da Hepatite B/fisiologia , Proteínas Proto-Oncogênicas c-sis/metabolismo , Receptor beta de Fator de Crescimento Derivado de Plaquetas/metabolismo , Actinas/genética , Actinas/metabolismo , Becaplermina , Proliferação de Células , Técnicas de Cocultura , Colágeno Tipo I/genética , Colágeno Tipo I/metabolismo , Células Hep G2 , Células Estreladas do Fígado/virologia , Interações Hospedeiro-Patógeno , Humanos , Cirrose Hepática/virologia , Fosforilação , Processamento de Proteína Pós-Traducional , Proteínas Proto-Oncogênicas c-sis/genética , Receptor beta de Fator de Crescimento Derivado de Plaquetas/genética , Transdução de Sinais , Regulação para Cima , Proteínas Virais/fisiologia
3.
Hepatol Res ; 42(9): 911-21, 2012 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-22524308

RESUMO

AIM: To investigate direct effects of hepatitis B virus (HBV) on collagen type I in vitro. METHODS: Collagen type I were measured after LX-2 cell cultured with purified or serum HBV for 12, 24 and 48 h. Furthermore, evidence of HBV infection to LX-2 were detected, and different inhibitors were used to identify pathways regulating collagen I expression. RESULTS: The 3 × 10(5) IU/mL purified/serum HBV increased collagen type I mRNA expression by 2.2-/3.2- and 1.3-/1.5-fold at 24 and 48 h, respectively. Collagen type I protein in the supernatant of purified/serum HBV group also increased compared to the control group (408.0 ± 8.0/384.4 ± 6.8 vs 262.7 ± 15.7 ng/mL, P < 0.05). However, the 3 × 10(7) IU/mL purified/serum HBV increased collagen type I expression similar to that of 3 × 10(5) IU/mL, while 3 × 10(3) IU/mL group showed no effect. Human HBV immunoglobulin alleviated HBV-induced collagen I expression, but no evidence of HBV infection was found. Neutralization of transforming growth factor beta, tumor necrosis factor alpha, platelet-derived growth factor, extracellular signal-regulated kinase and TGF-ß receptor had no obvious inhibitory effects; only inhibition of p38 mitogen-activated protein kinase decreased collagen type I mRNA expression by 0.5-/0.4- and 0.4-/0.3-fold at 24 and 48 h, respectively. It reduced collagen type I protein in the purified/serum HBV group for 48 h (252.1 ± 14.1/251.7 ± 18.8 vs 403.9 ± 4.9/385.0 ± 4.2 ng/mL, P < 0.05). CONCLUSION: HBV directly promotes collagen type I expression of LX-2 cells without infection in vitro.

4.
Mol Med Rep ; 4(5): 811-6, 2011.
Artigo em Inglês | MEDLINE | ID: mdl-21643627

RESUMO

Cyclooxygenase-2 (COX-2) is involved in the process of non-alcoholic steatohepatitis (NASH). However, the role of the COX-2 inhibitor in NASH has not yet been elucidated. Therefore, in the present study, we investigated the role of celecoxib in a rat model of NASH induced by a high-fat diet (HFD). Wistar rats were administered HFD by gavage, and rats administered normal saline by gavage served as the controls. After 4 weeks of HFD feeding, the rats were treated with celecoxib (20 mg/kg/day) or placebo for 4 weeks. At the end of 4 and 8 weeks, histological changes in the livers of the rats were analyzed using hematoxylin and eosin; blood was collected to detect biochemical indicators (serum aminotransferase and triglyceride). Liver triglyceride content was measured using the triglyceride E-test kit. The liver expression of COX-2, nuclear factor-κ enhancer binding protein (NF-κB) subunits p50 and p65 was measured by real-time reverse transcription-polymerase chain reaction and/or Western blotting. Infiltration of steatosis and inflammation in cells was observed in the livers after 4 weeks of HFD administration, and marked steatosis and inflammation was induced after 8 weeks. These histological changes were significantly attenuated after celecoxib treatment. Reduced serum alanine aminotransferase and triglyceride (TG) levels and TG content in the liver were observed in the HFD rats that received celecoxib. Moreover, celecoxib suppressed hepatic COX-2 messenger RNA and protein expression. The NF-κB subunit p50 and p65 protein levels in the HFD rats were also attenuated after celecoxib treatment. The results indicate that the induction of COX-2 occurs in association with NF-κB activation in HFD-induced NASH rats. Celecoxib may protect against the development of steatohepatitis induced by HFD.


Assuntos
Dieta , Fígado Gorduroso/complicações , Fígado Gorduroso/tratamento farmacológico , Inflamação/complicações , Inflamação/tratamento farmacológico , Pirazóis/uso terapêutico , Sulfonamidas/uso terapêutico , Alanina Transaminase/sangue , Animais , Celecoxib , Ciclo-Oxigenase 2/genética , Ciclo-Oxigenase 2/metabolismo , Gorduras na Dieta , Modelos Animais de Doenças , Fígado Gorduroso/sangue , Fígado Gorduroso/patologia , Regulação Enzimológica da Expressão Gênica/efeitos dos fármacos , Inflamação/sangue , Inflamação/patologia , Fígado/efeitos dos fármacos , Fígado/enzimologia , Fígado/patologia , NF-kappa B/metabolismo , Hepatopatia Gordurosa não Alcoólica , Pirazóis/farmacologia , Ratos , Ratos Wistar , Sulfonamidas/farmacologia , Triglicerídeos/sangue
SELEÇÃO DE REFERÊNCIAS
DETALHE DA PESQUISA
...