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1.
Journal of Southern Medical University ; (12): 1835-1837, 2008.
Artigo em Chinês | WPRIM | ID: wpr-321806

RESUMO

<p><b>OBJECTIVE</b>To investigate the effects of Scutellaria barbata extract (ESB) in suppressing tumor growth and modulating the immune functions in mice bearing tumors derived from hepatocarcinoma H22 cells.</p><p><b>METHODS</b>Fifty mice inoculated subcutaneously with H22 cells were equally divided into the model group, high-, moderate-, and low-dose ESB groups, and 5-Fu group, with corresponding treatments for 10 days. Another 10 mice with only saline injection served as the normal control group. The body weight, tumor mass, thymus index and spleen index of the mice were measured, and the lymphocyte proliferation activity, NK cell activity and interleukin-2 (IL-2) production by the splenocytes were detected.</p><p><b>RESULTS</b>Moderate- and high-dose ESB significantly suppressed the tumor growth with tumor inhibition rate of 28.68% and 36.98%, respectively. ESB treatment at moderate and high doses significantly increased the thymus index and spleen index (P < 0.01), which were decreased significantly in 5-Fu group. The lymphocyte proliferation activity, NK cell activity and IL-2 production by the splenocytes were significantly lower in the model group than in the normal group (P < 0.05). Compared with the model group, ESB at the high dose obviously increased the three indexes above mentioned. The NK cell activity was also significantly improved in moderate-dose ESB group (P < 0.05).</p><p><b>CONCLUSION</b>ESB can suppress the growth of H22 implant tumor and enhance the immune function of the tumor-bearing mice.</p>


Assuntos
Animais , Feminino , Masculino , Camundongos , Antineoplásicos Fitogênicos , Farmacologia , Medicamentos de Ervas Chinesas , Farmacologia , Interleucina-2 , Metabolismo , Células Matadoras Naturais , Alergia e Imunologia , Neoplasias Hepáticas Experimentais , Alergia e Imunologia , Patologia , Linfócitos , Alergia e Imunologia , Camundongos Endogâmicos ICR , Distribuição Aleatória , Scutellaria , Química
2.
Chinese Journal of Gastrointestinal Surgery ; (12): 261-265, 2008.
Artigo em Chinês | WPRIM | ID: wpr-273851

RESUMO

<p><b>OBJECTIVE</b>To investigate the mechanism of gastric carcinoma cells apoptosis induced by matrine injection in vitro.</p><p><b>METHODS</b>Effects of 24, 48, 72, 96 h incubation with different concentrations (0.25-1.5 g/L) of matrine injection on proliferation of SGC-7901 cells were evaluated using 3-4,5-dimethylthiazol-2-yl-2,5-diphenyltetrazolium bromide (MTT) assay. The cellular morphology of SGC-7901 cells was observed by transmission electron microscope (EM). Flow cytometry was used to analyze the apoptosis of SGC-7901 cells by staining with annexin V-FITC/PI. The expression of Fas/FasL was examined by flow cytometry using specific antibody. The activity of caspase-3 was measured by spectrofluorometry.</p><p><b>RESULTS</b>Matrine injection could inhibit the proliferation of SGC-7901 cells in a dose- and time-dependent manner. The typical morphological changes of apoptosis were observed after incubation with 1.0 g/L matrine injections for 48 h. The apoptosis rates of 0.5 g/L, 1.0 g/L and 1.5 g/L groups were 39.80%, 58.11% and 79.00% respectively. The apoptotic cells in matrine injection group were mainly early apoptotic cells, and those in 5-FU group were mainly late apoptotic cells and necrotic cells. Spectrofluorometry revealed FI levels of Fas and FasL were equal, which were both correlated with apoptosis rate. The activity of caspase-3 increased with the elevation of matrine concentration, and was correlated with the apoptosis rate.</p><p><b>CONCLUSION</b>Matrine injection can induce apoptosis of SGC-7901 cells through the up-regulation of Fas/FasL expression and activation of caspase-3.</p>


Assuntos
Humanos , Alcaloides , Farmacologia , Antineoplásicos Fitogênicos , Farmacologia , Apoptose , Caspase 3 , Metabolismo , Linhagem Celular Tumoral , Proteína Ligante Fas , Metabolismo , Proteínas Proto-Oncogênicas c-bcl-2 , Metabolismo , Quinolizinas , Farmacologia , Neoplasias Gástricas , Regulação para Cima , Receptor fas , Metabolismo
3.
Journal of Southern Medical University ; (12): 1397-1399, 2007.
Artigo em Chinês | WPRIM | ID: wpr-283121

RESUMO

<p><b>OBJECTIVE</b>To investigate the relationship between HER-2 expression and the efficacy of neoadjuvant chemotherapy in local advanced breast cancer.</p><p><b>METHODS</b>Different neoadjuvant chemotherapy regimens, namely CMF, CEF, and NEF, were administered in 132 patients with local advanced breast cancer for 2 cycles, each lasting for 28 days. According to the criteria recommended by WHO, the efficacy and safety of the regimens were evaluated after two cycles of neoadjuvant chemotherapy. HER-2 expression was examined by immunohistochemistry using specific monoclonal antibodies before chemotherapy and after surgery.</p><p><b>RESULTS</b>The overall response rate (RR) of CMF, CEF, and NEF regimens were 39.5% (17/43), 54.3% (25/46) and 72.1% (31/43), with incidence of leukopenia of 34.9% (15/43), 58.7% (27/46) and 60.5% (26/43), respectively. Other adverse effects including decreased hemoglobin (Hb) level, thrombocytopenia, gastrointestinal irritation and alopecia were similar between the 3 groups (P>0.05). No significant variation in HER-2 expression occurred after administration of the 3 regimens. The overall RR to CMF regimen in HER-2-negative breast cancer patients was significantly higher than that in HER-2-positive patients, but showed no significant difference with CEF and NEF regimens.</p><p><b>CONCLUSION</b>HER-2 expression is not decreased after neoadjuvant chemotherapy in breast cancer patients, and HER-2-positive breast cancer can be resistant to CMF regimen, but not to CEF and NEF regimens.</p>


Assuntos
Adulto , Idoso , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Neoplasias da Mama , Tratamento Farmacológico , Genética , Patologia , Terapêutica , Resistencia a Medicamentos Antineoplásicos , Regulação Neoplásica da Expressão Gênica , Terapia Neoadjuvante , Métodos , Receptor ErbB-2 , Metabolismo , Resultado do Tratamento
4.
Journal of Southern Medical University ; (12): 1599-1602, 2006.
Artigo em Chinês | WPRIM | ID: wpr-232828

RESUMO

<p><b>OBJECTIVE</b>To evaluate the chemopreventive effect of celecoxib, a specific cyclooxegenease-2 (COX-2) inhibitor, on chemically induced breast cancer of rats and its effect on COX-2 expression.</p><p><b>METHODS</b>7, 12-dimethylbenz anthracene (DMBA) was administered intragastrically in SD female rats to establish breast cancer models, which were divided subsequently into control group, tamoxifen group and celecoxib group to receive different treatments accordingly. The occurrence rate of breast cancer was observed and the effect of celecoxib on COX-2 and vascular endothelial growth factor (VEGF) expressions assayed by immunohistochemical SP method.</p><p><b>RESULTS</b>The incidence of breast cancer in tamoxifen group (48.15%) and celecoxib group (50.00%) were both significantly lower than that in the control group (85.71%; P=0.003 and P=0.004, respectively). The positivity rate of COX-2 expression in celecoxib group (28.57%) was significantly lower than those of tamoxifen group (48.15%) and control group (83.33%; P=0.001 and P=0.035, respectively). The positivity rate of VEGF expression in celecoxib group (42.86%) was significantly lower than that of control group (79.17%, P=0.023), but comparable with that in tamoxifen group (46.15%, P=0.863).</p><p><b>CONCLUSION</b>Celecoxib can significantly suppress DMBA-induced breast cancer in female rats possibly through down-regulation of COX-2 and VEGF expressions.</p>


Assuntos
Animais , Feminino , Ratos , 9,10-Dimetil-1,2-benzantraceno , Celecoxib , Ciclo-Oxigenase 2 , Metabolismo , Inibidores de Ciclo-Oxigenase , Usos Terapêuticos , Regulação para Baixo , Imuno-Histoquímica , Neoplasias Mamárias Experimentais , Metabolismo , Pirazóis , Usos Terapêuticos , Ratos Sprague-Dawley , Sulfonamidas , Usos Terapêuticos , Tamoxifeno , Usos Terapêuticos , Resultado do Tratamento , Fator A de Crescimento do Endotélio Vascular , Metabolismo
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