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J Dig Dis ; 8(3): 154-9, 2007 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-17650228


OBJECTIVE: To investigate the effects of inflammatory cytokines, tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), interleukin-6 (IL-6) and vascular cell adhesion molecule (VCAM-1), on the recurrence of liver cancer after apparently curative surgical resection of the tumor. METHODS: An experimental mouse model of liver cancer metastasis was designed using hepatoma 22(H(22)) inoculated into the subserous layer of spleen of 615 mice. Partial hepatectomy (PH) or sham operation (SH) was performed at various periods of spleen inoculation and metastasic effects were recorded. The expression of inflammatory cytokines as TNF-alpha, IL-1beta, IL-6 and VCAM-1 were analyzed by reverse transcriptase-polymerase chain reaction (RT-PCR). RESULTS: Compared with SH, a significant augmented metastatic effect was observed in the mice with PH (P < 0.01), and higher mRNA expressions of TNF-alpha, IL-1beta, IL-6 and VCAM-1 were also observed. The peak expressions of IL-1beta, IL-6 and VCAM-1 were found at 48 and 72 h, respectively. Among them, TNF-alpha expression was found immediately increasing after 4 h and kept at a high level till 96 h after PH. The expression of VCAM-1 was found to have two peaks at 4 and 72 h after PH, 3-6 times higher than its level prior to the operation. The expression of TNF-alpha, IL-1beta, IL-6 and VCAM-1 showed a significantly positive correlation with the augmenting effect of liver metastasis in the mice model. CONCLUSION: The results indicate that pro-inflammatory cytokines, TNF-alpha, IL-1beta, IL-6 and VCAM-1 might be involved in promoting the enhanced metastasis of liver cancer after surgical operation, especially the PH.

Carcinoma Hepatocelular/imunologia , Citocinas/fisiologia , Neoplasias Hepáticas/imunologia , Recidiva Local de Neoplasia/imunologia , Neoplasias Esplênicas/imunologia , Animais , Carcinoma Hepatocelular/secundário , Modelos Animais de Doenças , Feminino , Hepatectomia , Neoplasias Hepáticas/patologia , Neoplasias Hepáticas/cirurgia , Camundongos , Neoplasias Esplênicas/secundário
Chin J Dig Dis ; 6(2): 93-7, 2005.
Artigo em Inglês | MEDLINE | ID: mdl-15904428


OBJECTIVE: The goal of the present study was to determine how proapoptosis proteins regulate the progression of liver proliferative foci and tumorigenesis initiated by a chemical carcinogen, diethylnitrosamine (DEN). METHODS: Bid-deficient mice (15-day-old) were injected with 15 microg/g of DEN, then killed at 3 and 10 days, and 4 and 8 months after injection for analysis of hepatocellular proliferation, apoptosis and tumorigenesis. RESULT: The rate of apoptosis in the hepatocytes of the wild-type mice was significantly higher than in the Bid-deficient mice at 10 days after DEN exposure (P < 0.0001); the results of BrdU labeling agreed with the measurement of apoptosis in these animals, showing an obvious increase in the wild-type mice compared with the Bid-deficient mice (P < 0.0001). Four months after DEN exposure, the number and size of lesion foci or nodules in the wild-type mice were both greater than in the Bid-deficient mice (P < 0.05 and P < 0.001, respectively), but there was no significant difference between the two groups of mice at 8 months. CONCLUSION: These results suggest that a lack of apoptosis in liver tissue in the early stage after DEN exposure decreased some of the tumorigenesis potential of DEN.

Apoptose/fisiologia , Proteínas de Transporte/fisiologia , Neoplasias Hepáticas/fisiopatologia , Animais , Proteína Agonista de Morte Celular de Domínio Interatuante com BH3 , Proliferação de Células , Dietilnitrosamina/efeitos adversos , Progressão da Doença , Hepatócitos/fisiologia , Marcação In Situ das Extremidades Cortadas , Neoplasias Hepáticas/induzido quimicamente , Camundongos , Camundongos Knockout
Chin J Dig Dis ; 5(4): 175-80, 2004.
Artigo em Inglês | MEDLINE | ID: mdl-15612888


OBJECTIVE: To investigate the mechanism of hepatocyte apoptosis induced by the proapoptosis protein Bid. METHODS: Mouse primary hepatocytes were isolated from wild-type and Bid-deficient mice and treated with tumor necrosis factor-alpha (TNF-alpha) or anti-Fas antibody to induce cell apoptosis. Immunofluorescence staining of Bax was performed to recognize Bax translocation and its conformational change. The wild-type mice or wild-type mice transfected with the adenovirus carried DN-FADD (Dominant Negative-Fas Associated Death Domain) and the Bid-deficient mice were injected with anti-Fas antibody 2 h before being killed. Caspase 3 and 8 activities were measured. Bands of Bid cleavage and Bax conformational change were detected by Western blot. RESULTS: Death receptors, including TNF-alpha and anti-Fas antibody, induced hepatocytes apoptosis, Bax translocation and conformational change through activation of Bid, which caused Bax to be inserted into the mitochondrial membrane of hepatocytes. The translocation and insertion of Bax were blocked when Bid was knocked out or blocked, and hepatocyte apoptosis was delayed or inhibited. CONCLUSION: Hepatocyte apoptosis induced by death receptors is regulated by Bid and the translocation and insertion of Bax are also dependent on Bid.

Apoptose , Proteínas de Transporte/farmacologia , Hepatócitos/efeitos dos fármacos , Hepatócitos/fisiologia , Animais , Proteína Agonista de Morte Celular de Domínio Interatuante com BH3 , Genes bcl-2 , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Fragmentos de Peptídeos , Proteínas Proto-Oncogênicas c-bcl-2 , Translocação Genética , Proteína X Associada a bcl-2 , Receptor fas