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Mol Med Rep ; 14(5): 4198-4208, 2016 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-27748914


Human glioma is the most common type of primary brain tumor and one of the most invasive and aggressive tumors, which, even with treatments including surgery, radiotherapy and chemotherapy, often relapses and exhibits resistance to conventional treatment methods. Developing novel strategies to control human glioma is, therefore, an important research focus. The present study investigated the mechanism of apoptosis induction in U251 human glioma cells by capsaicin (Cap) and dihydrocapsaicin (DHC), the major pungent ingredients of red chili pepper, using the Cell Counting Kit­8 assay, transmission electron microscopy analysis, flow cytometry analysis, laser scanning confocal microscope analysis and immunohistochemical staining. Treatment of U251 glioma cells with Cap and DHC resulted in a dose­ and time­dependent inhibition of cell viability and induction of apoptosis, whereas few effects were observed on the viability of L929 normal murine fibroblast cells. The apoptosis­inducing effects of Cap and DHC in U251 cells were associated with the generation of reactive oxygen species, increased Ca2+ concentrations, mitochondrial depolarization, release of cytochrome c into the cytosol and activation of caspase­9 and ­3. These effects were further confirmed by observations of the anti­tumor effects of Cap and DHC in vivo in a U251 cell murine tumor xenograft model. These results demonstrate that Cap and DHC are effective inhibitors of in vitro and in vivo survival of human glioma cells, and provide the rationale for further clinical investigation of Cap and DHC as treatments for human glioma.

Apoptose/efeitos dos fármacos , Capsaicina/análogos & derivados , Capsaicina/administração & dosagem , Glioma/tratamento farmacológico , Recidiva Local de Neoplasia/tratamento farmacológico , Animais , Sinalização do Cálcio/efeitos dos fármacos , Capsaicina/química , Capsicum/química , Linhagem Celular Tumoral , Proliferação de Células/efeitos dos fármacos , Glioma/genética , Glioma/patologia , Humanos , Camundongos , Mitocôndrias/genética , Recidiva Local de Neoplasia/genética , Recidiva Local de Neoplasia/patologia , Espécies Reativas de Oxigênio/metabolismo , Ensaios Antitumorais Modelo de Xenoenxerto
Zhonghua Nan Ke Xue ; 9(5): 327-30, 2003 Aug.
Artigo em Chinês | MEDLINE | ID: mdl-14513635


OBJECTIVE: To explore the effect of electromagnetic pulse (EMP) irradiation on structure and function of Leydig cells in mice. METHODS: One hundred and fourteen male Kunming mice were randomly divided into irradiated and control group, the former radiated generally by 8 x 10(3) V/m, 2 x 10(4) V/m and 6 x 10(4) V/m EMP respectively five times within two minutes. Pathological changes of Leydig cells were observed by light and electron microscope. Serum testosterone (T), luteinizing hormone (LH) and estradiol (E2) were measured dynamically by radioimmunoassay at 6 h, 1 d, 3 d, 7 d, 14 d and 28 d after irradiation. RESULTS: Main pathological changes were edema and vacuolation, swelling of cytoplasmic mitochondria, reduce of lipid droplets, pale staining of most of lipid droplets, and partial or complete cavitation of lipid droplets in Leydig cells within 28 days after EMP radiation. Compared with normal controls, serum T decreased in all in different degrees within 28 days, and dropped significantly at 6 h-14 d, 6 h-7 d and 1 d-28 d after 8 x 10(3) V/m, 2 x 10(4) V/m and 6 x 10(4) V/m EMP irradiation(P < 0.05 or P < 0.01). EMP irradiation caused no significant changes in serum LH and E2. CONCLUSIONS: Leydig cells are among those that are the most susceptible to EMP irradiation. EMP irradiation may cause significant injury in structure and function of Leydig cells in mice, whose earlier and continuous effect is bound to affect sexual function and sperm production.

Fenômenos Eletromagnéticos , Células Intersticiais do Testículo/efeitos da radiação , Animais , Relação Dose-Resposta à Radiação , Estradiol/sangue , Hormônios/sangue , Células Intersticiais do Testículo/patologia , Hormônio Luteinizante/sangue , Masculino , Camundongos , Camundongos Endogâmicos , Distribuição Aleatória , Testosterona/sangue